PARKINSON'S DISEASE NEWS
Parkinson's Disease News covers all significant new research, reports, books, and resources concerning Parkinson's Disease. Articles are chosen on the basis of their medical significance or potential interest. Our overwhelming priority is the facts, regardless of whether they contradict prevailing views or vested interests. Analysis and further information are provided either to explain the background or implications, or to balance misleading claims. If you notice errors or inadequacies, or dispute what is written, or want to propose articles, please e-mail firstname.lastname@example.org.
2nd September 2017 - New research
ASTHMATIC INHALER FOR PARKINSON'S DISEASE
Salbutamol, which is normally used in inhalers for asthma, was found to reduce the risk of Parkinson's Disease by a third. Those people taking higher doses were half as likely to develop Parkinson's Disease. Salbutamol is a β2-adrenoreceptor (β2AR) agonist, which is also a regulator of the α-synuclein gene (SNCA). Alpha-synuclein can accumulate in Parkinson's Disease. Consequently, it has been suggested that salbutamol reduces the risk of Parkinson's Disease by lowering the levels of α-synuclein. However, α-synuclein does not cause Parkinson's Disease. It is Parkinson's Disease that can cause an accumulation of α-synuclein. The effect of Salbutamol on people with Parkinson's Disease may be due to β2-adrenoreceptor (β2AR) agonists also having an anti-cholinergic effect. Anti-cholinergics are drugs used for Parkinson's Disease.
Reference : Science  357 (6354) : 891-898 (S.Mittal, K.Bjørnevik, D.S.Im, A.Flierl, X.Dong, J.J.Locascio, K.M.Abo, E.Long, M.Jin, B.Xu, Y.K.Xiang, J.C.Rochet, A.Engeland, P.Rizzu, P.Heutink, T.Bartels, D.J.Selkoe, B.J.Caldarone, M.A.Glicksman, V.Khurana, B.Schüle, D.S.Park, T.Riise, C.R.Scherzer) Complete abstract
26th August 2017 - News release
GOCOVRI™ APPROVED FOR DYSKINESIA IN PARKINSON'S DISEASE
Adamas Pharmaceuticals announced that the U.S. Food and Drug Administratio (FDA) has approved GOCOVRI (274mg amantadine) extended release capsules (previously ADS-5102) for the treatment of dyskinesia in people with Parkinson's Disease receiving L-dopa based therapy, with or without additional dopaminergic medications.
GOCOVRI is expected to be available in the fourth quarter, and be formally launched with the Adamas's sales force in January 2018. In clinical studies GOCOVRI caused a 37% to 46% reduction in the Unified Dyskinesia Rating Scale compared to 12% to 16% for a placebo. GOCOVRI-treated patients also experienced a 3.6 and 4.0 hour increase in functional time daily (defined as ON time without troublesome dyskinesia) vs. a 0.8 and 2.1 hour increase for placebo-treated patients at Week 12. The most common adverse effects were hallucinations, dizziness, dry mouth, fall, peripheral edema, constipation, and orthostatic hypotension. For the news release go to : News release
19th August 2017 - New research
FAILED FACIAL EXPRESSION IN PARKINSON'S DISEASE
People with Parkinson's Disease commonly have impairment of facial expressivity (hypomimia) and also have difficulties in interpreting the emotional facial expressions of other people, especially for aversive emotions. The ability of recognising emotional facial expressions by people with Parkinson's Disease was assessed using the Ekman 60-faces test (Emotion recognition task).
For emotion recognition, people with Parkinson's Disease reported lower scores than average. There was a particular difficulty by people with Parkinson's Disease in recognising certain emotions including happiness, fear, anger, sadness and surprise. With showing facial emotions people with Parkinson's Disease differed from normal, especially regarding happiness, sadness, and anger, which were displayed by them less than normal. There was a relationship between emotion facial recognition and facial expression in people with or without Parkinson's Disease. So it appears that they go together.
The correlation between the recognition of emotions and the expression of emotions suggests that they share a common cause, which could be deteriorated in people with Parkinson's Disease.
Reference : PLoS One  12 (1) : e0169110 (L.Ricciardi, F.Visco-Comandini, R.Erro, F.Morgante, M.Bologna, A.Fasano, D.Ricciardi, M.J.Edwards, J.Kilner) Complete abstract In order to refer to this article on its own click here
13th August 2017 - New research
OCCUPATIONAL PESTICIDE USE IN PARKINSON'S DISEASE
Researchers assessed the influence of occupational pesticide use on the prevalence of Parkinson's Disease in people with information available concerning occupational, residential, and household sources of pesticide exposure.
Ever having used carbamate pesticides increased the risk of Parkinson's Disease by 455%, while the use of organophosphorus pesticides (OP) and organochlorine pesticides (OC) doubled the risk of Parkinson's Disease. The risk of developing Parkinson's Disease increased by 110% to 211% if somebody had ever had occupational use of fungicides, herbicides, and insecticides. Using any pesticide occupationally for more than 10 years doubled the risk of Parkinson's Disease compared with those people that had no occupational pesticide use.
Most surprisingly, the researchers estimated higher risks of Parkinson's Disease among those people reporting use of personal protective equipment (PPE). This suggests that personal protective equipment is insufficient for protection against pesticides.
8th August 2017 - New book
THE ENLIGHTENED MR. PARKINSON : THE PIONEERING LIFE OF A FORGOTTEN SURGEON
Publisher's description : In 1817 - two hundred years years ago - James Parkinson (1755–1824) defined this mysterious ailment so precisely that we still diagnose Parkinson's Disease today by recognizing the symptoms he identified. The story of this remarkable man’s contributions to the Age of the Enlightenment is told through his three seemingly disparate passions: medicine, politics and fossils. As a political radical, Parkinson was interrogated over a plot to kill King George III and was in danger of exile. But simultaneously, he was helping Edward Jenner set up smallpox vaccination stations across London and writing the first scientific study of fossils in English, jump-starting a national craze. He is one of the pioneers of "the age of wonder," forgotten to history. The author restores him to his rightful place in history with her evocative portrait of the man and his era. Click here for more details For more books concerning Parkinson's Disease go to Parkinson's Disease books
4th August 2017 - New research
DIABETIC DRUG ASSESSED FOR USE IN PARKINSON'S DISEASE
Exenatide is a type 2 diabetes treatment that differs in its pharmacological action and structure from insulin. Exenatide is an injected glucagon-like peptide-1 agonist. The possible means of how it might affect Parkinson's Disease is not known. It has no direct effect on dopamine.
The effects of exenatide were assessed in people with moderate Parkinson's Disease. The primary outcome was the adjusted difference in the Movement Disorders Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor subscale (part 3). After over a year, off-medication scores on part 3 of the MDS-UPDRS had improved by only 1·0 point in people taking exentaide and worsened in people taking a placebo. Although it has been claimed that exenatide can slow down Parkinson's Disease the efficacy is too mild to justify such claims. Injection site reactions and gastrointestinal symptoms were common adverse events in both groups.
In four previous studies the efficacy was also found to be mild. Unusually, the effects of exenatide on Parkinson's Disease had continued to some extent beyond its use. In those studies exenatide was well tolerated but weight loss was common. Other adverse effects of the use of exenatide were nausea, injection-site induration, dyslipidemia, vomiting, diarrhoea, headache and hypoglycaemia.
The Lancet  S0140-6736(17)31585-4390 (D.Athauda, K.Maclagan,
S.S.Skene, M.Bajwa-Joseph, D.Letchford, K.Chowdhury, S.Hibbert, N.Budnik,
L.Zampedri, J.Dickson, Y.Li, I.Aviles-Olmos, T.T.Warner, P.Limousin,
A.J.Lees, N.H.Greig, S.Tebbs, T.Foltynie)
In order to refer to this article on its own
1st August 2017 - New research
NEW DOPAMINE AGONIST BEING ASSESSED FOR PARKINSON'S DISEASE
D-512 is a new dopamine agonist presently being assessed for its possible use in Parkinson's Disease. Parkinson's Disease is often treated using dopamine agonists such as ropinirole. Ropinirole stimulates the D2 and D3 dopamine receptors. However, dopamine agonists tend to lose efficacy over time and do not prevent the progression of Parkinson's Disease. D-512 also stimulates D2 and D3 dopamine receptors but is also claimed to have antioxidant and other neuroprotective properties. In an animal study D-512 was shown to have superior peak-dose efficacy and a longer duration of action than ropinirole, despite having similar side-effects. Consequently, D-512 has the potential for future use as a dopamine agonist for the treatment of Parkinson's Disease.
Reference : British Journal of Pharmacology  Jul 1 [Epub ahead of print] (D.Lindenbach, B.Das, M.Conti, S.M.Meadows, A.K.Dutta, C.Bishop) Complete abstract
29th July 2017 - News release
CLINICAL TRIAL OF FOLIGLURAX FOR PARKINSON'S DISEASE
Prexton Therapeutics have announced the launch of phase II clinical testing of Foliglurax in people with Parkinson’s Disease. The results of a phase I clinical trial showed that Foliglurax was safe and well-tolerated.
The clinical study will evaluate 165 patients in sites across six European countries (UK, Germany, France, Austria, Spain and Italy), starting in July 2017. The study is double-blind, randomised, and placebo-controlled in people who are experiencing the wearing-off of L-dopa and L-dopa-Induced Dyskinesia (LID). The clinical trial will assess the safety and tolerability, and efficacy of Foliglurax. Instead of affecting dopamine, Foliglurax stimulates a novel compensatory neuronal system that activates a specific glutamatergic system target (mGluR4) that is unaffected by Parkinson's Disease. For the news release go to : News release
25th July 2017 - New research
CANNABIS USE IN PARKINSON'S DISEASE
Cannabis has been widely used to help people cope with Parkinson's Disease. Different parts of the plant that are used for pharmacological purposes are cannabis, marijuana and hashish. The main pharmacological constituents are Cannabinoids. For more information go to : Cannabis Current users have reported a high level of efficacy, averaging 6.4 on a scale of 0 to 7. Around 59% of them reported reducing prescription medication since beginning cannabis use. Current cannabis users were younger and less likely to be classified as obese. Cannabis users also reported lower levels of disability, specifically in domains of mood, memory, and fatigue.
Reference : Complementary Therapies in Medicine  33 : 99-104 (J.H.Kindred, K.Li, N.B.Ketelhut, F.Proessl, B.W.Fling, J.M.Honce, W.R.Shaffer, T.Rudroff) Complete abstract
21st July 2017 - New research
THE GUT BRAIN AXIS IN PARKINSON'S DISEASE
Enterin have obtained considerable finance in order to fund the ongoing Phase 1/2a clinical trial targeting the accumulation of alpha-synuclein in the enteric nervous system. The trial is examining the safety, tolerability, pharmacokinetics, and pharmacodynamics of ENT-01 to relieve constipation in Parkinson’s Disease. They are also monitoring symptoms such as sleep, REM-behavior disorder, depression, fatigue and even motor symptoms. ENT-01 is an oral drug that contains a derivative of squalamine. Squalamine can inhibit the aggregation of alpha-synuclein. For more information go to : Enterin They claim that this could lead to the treatment of Parkinson's Disease.
However, it is Parkinson's Disease, due to low L-dopa that ultimately causes alpha-synuclein formation, not alpha-synuclein that causes Parkinson's Disease. They also claim that Parkinson's Disease originates in the gut and travels to the brain. However, the fault in Parkinson's Disease is the insufficient activity of the dopaminergic neurons in the brain. There are no dopaminergic neurons in the gut. Dopaminergic neurons can not travel to the brain. Dopamine produced in the gut, which can only be produced by bacteria, can not enter the brain.
22nd June 2017 - New research
AUTOIMMUNITY AND PARKINSON'S DISEASE
Researchers have claimed that they have found evidence that autoimmunity has a role in causing Parkinson's Disease. They suggest that fragments of alpha-synuclein, which can accumulate in people with Parkinson's Disease, trigger an immune response that kills the cells that produce dopamine. However, their theory is fundamentally flawed. When there is insufficient formation of L-dopa, which is what occurs in Parkinson's Disease, iron accumulation and superoxide anion can be formed. Both of these increase the formation and aggregation of alpha-synuclein. So it is Parkinson's Disease, due to low L-dopa that ultimately causes alpha-synuclein formation, not alpha-synuclein that causes Parkinson's Disease. For more information go to the : Complete abstract
12th June 2017 - News release
CDNF CLINICAL TRIAL FOR PARKINSON'S DISEASE
Herantis Pharma have been authorised to carry out a randomized clinical trial on the use of CDNF in the treatment of Parkinson's Disease. The clinical trials will be carried out in Sweden and Finland. CDNF is Cerebral Dopamine Neurotrophic Factor, which is a natural protein produced in brain cells, that is claimed to have neuroprotective and neurorestorative properties. In preclinical studies including chronic toxicology studies, CDNF has been found to be safe. CDNF protected and regenerated cells that produce dopamine. CDNF has also shown efficacy in non-motor symptoms of Parkinson's Disease. For the news release go to : News release
7th June 2017 - New research
WIRELESS DEEP BRAIN STIMULATION FOR PARKINSON'S DISEASE
Deep brain stimulation (DBS) is the most commonly performed and most effective surgery for Parkinson's Disease but is unaffordable to a lot of people. It involves the use of electrodes implanted into the brain connected to an electrical device. For more information go to : Deep Brain Stimulation
A novel wireless method of administering brain stimulation has been introduced that requires no implants or external connections. By injecting magnetic nanoparticles into the brain, neurons can be manipulated by applying external magnetic fields. These particles are capable of deep penetration of brain tissue and can stimulate nerve cells. For more information go to : Wireless Deep Brain Stimulation
Reference : Stereotactic and Functional Neurosurgery  95 (3) : 174-182 [Epub ahead of print] (D.Li, C.Zhang, J.Gault, W.Wang, J.Liu, M.Shao, Y.Zhao, K.Zeljic, G.Gao, B.Sun) Complete abstract In order to refer to this article on its own click here
4th June 2017 - New research
AIR POLLUTION INCREASES THE RISK OF PARKINSON'S DISEASE
Researchers investigated the effects of air pollution on the risk of Parkinson's Disease. They primarily assessed atmospheric particulate matter (PM), which are solid or liquid matter that is suspended in the atmosphere. Sources of particulate matter can be man-made or natural, and can very adversely affect human health. It includes particles such as dust, pollen, soot, smoke, and liquid droplets. Also assessed was nitrogen dioxide (NO2), which is a prominent air pollutant. Nitrogen dioxide is formed during the industrial synthesis of nitric acid, millions of tons of which are produced each year.
29th May 2017 - New research
CLINICAL TRIAL OF SAFINAMIDE FOR PARKINSON'S DISEASE
Safinamide has both dopaminergic properties (highly selective and reversible inhibition of monoamine oxidase-B) and non-dopaminergic properties (selective sodium channel blockade and calcium channel modulation, with consequent inhibition of excessive glutamate release). It is usually added to the use of L-dopa or dopamine agonists. For more information go to Xadago : Xadago
Reference : JAMA Neurology  74 (2) : 216-224 (A.H.Schapira, S.H.Fox, R.A.Hauser, J.Jankovic, W.H.Jost, C.Kenney, J.Kulisevsky, R.Pahwa, W.Poewe, R.Anand) Complete abstract
17th May 2017 - New research
LIQUID L-DOPA FOR PARKINSON'S DISEASE
Liquid L-dopa is usually taken as a combination of L-dopa, carbidopa, and ascorbic acid (vitamin C) in a solution called LCAS. Therapy with liquid L-dopa has been used in people with advanced Parkinson's Disease for many years. However, long-term follow-up information is scarce. The present study aimed to determine the long-term retention rate for LCAS therapy, and to identify the causes of LCAS therapy withdrawal.
Reference : Journal of Neurological Science  377 : 6-11 (H.J.Yang, G.Ehm, Y.E.Kim, J.Y.Yun, W.W.Lee, A.Kim, H.J.Kim, B.Jeon) Complete abstract
16th April 2017 - New research
PREVALENT ESOPHAGEAL SYMPTOMS IN PARKINSON'S DISEASE
Dysphagia (difficulty in swallowing) is a common problem in people with Parkinson's Disease. In order to assess the prevalence of dysphagia and other related symptoms, people with Parkinson's Disease presenting with dysphagia, odynophagia, heartburn, regurgitation, chest pain, and weight loss underwent evaluation using high-resolution manometry (HRM).
Reference : Diseases of the Esophagus  30 (4) : 1-6 (A.Su, R.Gandhy, C.Barlow, G.Triadafilopoulos) Nature Biotechnology  Apr 10 [Epub ahead of print] Complete abstract
12th April 2017 - New research
DOPAMINERGIC NEURONS MADE FROM ASTROCYTES
Dopaminergic neurons, the cells involved in Parkinson's Disease, have been directly converted from astrocytes, which are a completely different type of cell. The source of the cells were humans, and mice who did not have Parkinson's Disease. This is different from previous methods, which have aimed at transplanting the cells affected by the pathological process. The aim of the treatment is to eventually treat Parkinson's Disease.
The theory behind trying to replace the dopaminergic neurons in Parkinson's Disease is the assumption that there is a massive loss of the cells involved in Parkinson's Disease, and that the cells therefore need replacing. However, although it is widely believed that there is massive cell loss in Parkinson's Disease not a single study has ever shown this to be true. The study from which these claims originate showed that there was a major reduction in the activity of the cells involved in Parkinson's Disease, not a major loss of cells. Consequently, any method aimed at replacing dopaminergic neurons does not have a sound scientific basis, and so would inevitably fail as have all attempts at ridding Parkinson's Disease by replacing dopaminergic neurons. In order to refer to this article on its own click here
Reference : Nature Biotechnology  Apr 10 [Epub ahead of print] (P.R.di Val Cervo, R.A.Romanov, G.Spigolon, D.Masini, E.Martín-Montañez, E.M.Toledo, G.La Manno, M.Feyder, C.Pifl, Y.H.Ng, S.P.Sánchez, S.Linnarsson, M.Wernig, T.Harkany, G.Fisone, E.Arenas) Complete abstract
11th April 2017
WORLD PARKINSON'S DISEASE DAY
The 11th April every year is designated as World Parkinson's Disease Day. The aim of World Parkinson's Disease Day is to raise public awareness of Parkinson's Disease, a medical disorder that begins mildly but that can end up having serious and widespread effects that affect every system in the body.
The 11th April is chosen because it is the birthday of James Parkinson after whom Parkinson's Disease is named. Contrary to common belief, James Parkinson did not discover Parkinson's Disease. The symptoms of Parkinson's Disease have been known and treated since ancient times. Despite all the claimed breakthroughs since then, there are now up to 10 million people with Parkinson's Disease. Tens of millions of people more who are alive right now will eventually have Parkinson's Disease. However, this is the last century in which Parkinson's Disease will exist. The likely future of Parkinson's Disease is that it will be readily and accurately diagnosed, and effectively treated without side effects, before its characteristic symptoms even become apparent. In order to refer to this article on its own click here
9th April 2017 - New research
DEXTROMETHORPHAN FOR PARKINSON'S DISEASE DYSKINESIA
Dextromethorphan/quinidine, whose trade name Nuedexta, is a combination drug containing dextromethorphan and the antiarrhythmic agent quinidine. Quinidine is included to inhibit dextromeththorphan metabolism. For more information go to Nuedexta This pilot-study (NCT01767129) examined the safety and efficacy of dextromethorphan plus quinidine for treating L-dopa induced dyskinesia. People with Parkinson's Disease were randomised to 45mg dextromethorphan and 10mg twice daily, alternated with a placebo.
The main assessment was dyskinesia severity. Dyskinesia severity was a bit lower with dextromethorphan and quinidine than with a placebo, and subsequently significantly lower. Most of the patients rated their dyskinesia "much or very much improved" when taking dextromethorphan and quinidine. Dextromethorphan and quinidine did not worsen Parkinson's Disease motor scores, was generally well tolerated, but was associated with more frequent adverse effects. This study provides preliminary evidence of clinical benefit with dextromethorphan / quinidine for treating L-dopa induced dyskinesia in Parkinson's Disease. Larger and longer studies are needed to corroborate these findings.
Reference : Movement Disorders  Mar 30 [Epub ahead of print] (S.H.Fox, L.V. Metman, J.G.Nutt, M.Brodsky, S.A.Factor, A.E.Lang, L.E.Pope, N.Knowles, J.Siffert) Complete abstract In order to refer to this article on its own click here
7th April 2017 - New research
P2B 001 (RASAGILINE AND PRAMIPEXOLE) FOR PARKINSON'S DISEASE
P2B 001 is a novel combination of (1) slow release and (2) low dose rasagiline and pramipexole for synergistic use in early Parkinson's Disease that is presently in development. For more information go to P2B 001 Rasagiline is a MAO inhibitor for use in treating Parkinson's Disease. For more information go to Rasagiline Pramipexole is a dopamine agonist that is also for use in Parkinson's Disease. For more information go to : Pramipexole
People with early Parkinson's Disease were assessed when taking either : P2B 001 (0.3mg pramipexole / 0.75mg rasagiline), P2B001 (0.6mg pramipexole / 0.75mg rasagiline) or a placebo. The most effective of these was P2B 001 with a higher dose of pramipexole, followed by P2B 001 with a lower dose of pramipexole. Significant benefits were observed for both doses in : Parkinson Disease Quality of Life Scale-39 scores, the UPDRS (Parkinson's Disease) motor score, and activities of daily living. The adverse effects of P2B 001 were comparable to the use of a placebo apart from transient nausea and somnolence, which were more common with P2B 001 treatment. The researchers suggest that P2B 001 offers a promising treatment option for use in early Parkinson's Disease with good clinical efficacy and a low risk of adverse effects, in a way that can not be achieved by taking each drug on their own.
Reference : Movement Disorders  Apr 3 [Epub ahead of print] (C.W.Olanow, K. Kieburtz, M.Leinonen, L.Elmer, N.Giladi, R.A.Hauser, O.S.Klepiskaya, D.L.Kreitzman, M. F.Lew, D.S.Russell, S.Kadosh, P.Litman, H.Friedman, N.Linvah) Complete abstract In order to refer to this article on its own click here
4th April 2017 - New research
POSTURAL DEFORMITIES IN PARKINSON'S DISEASE
Striatal (hand and foot) and postural deformities are known to commonly occur in people with atypical Parkinsonism, but also occur in people with Parkinson's Disease. These deformities are frequently misdiagnosed as joint or orthopaedic problems that can often lead to unnecessary investigations. For more information go to : Postural deformities
Various striatal (hand and foot) and postural deformities (antecollis, camptocormia, scoliosis and Pisa syndrome) and their relation with the duration of Parkinson's Disease, severity and L-dopa intake were analyzed. Of those people with Parkinson's Disease, nearly half of them (48.5%) had either striatal or postural deformities. Striatal foot deformities were the most common deformity observed (25%). Camptocormia was the second most common deformity (20%). Striatal and postural deformities were seen in more advanced Parkinson's Disease as suggested by higher UPDRS scores. Striatal deformities almost always (94%) occurred on the same side of the body as the onset of Parkinson's Disease symptoms. Pisa and scoliosis occurred more (66%) on the opposite side to the onset of Parkinson's Disease symptoms.
The results showed that striatal and postural deformities were common and present in about half of the people with Parkinson's Disease. These deformities we more common in people in the advanced stages of Parkinson's Disease.
27th March 2017 - New research
HIGHER RISK OF MALNUTRITION IN PARKINSON'S DISEASE
People with Parkinson's Disease are known to be at a higher risk of malnutrition. The prevalence of malnutrition in Parkinson's Disease has been estimated to be up to 24%. Between 3% and 60% of people with Parkinson's Disease are reported to be at risk of malnutrition. To date, there is no clear explanation for malnutrition in these patients.
The aim of this study was to determine the prevalence of malnutrition and the factors that cause it. Of the patients they assessed, 55% of them were at risk of malnutrition, and 8% of them had already been malnourished. Age, Parkinson's Disease severity, off periods, depression and hypothyroidism were the factors most related to developing malnutrition. The dopamine agonist ropinirole was one of the factors that was most associated with a more favourable nutritional status.
Dopamine, whose deficiency causes Parkinson's Disease, is made from dietary substances, including vitamins, minerals and L-tyrosine, which is usually obtained from high protein foods. The deficiency of any of these nutrients could consequently lessen the amount of dopamine produced. The malnutrition that is common in Parkinson's Disease could therefore not only contribute to its onset but could worsen the symptoms over time even further.
Reference : Journal of Neurological Science  375 : 235-238 (S.Tomic, V.Pekic, Z. Popijac, T.Pucic, M.Petek, T.G.Kuric, S.Misevic) Complete abstract In order to refer to this article on its own click here
25th March - News release
XADAGO APPROVED FOR PARKINSON'S DISEASE
Newron Pharmaceuticals have announced that the U.S. Food and Drug Administration has approved its Parkinson's Disease treatment Xadago as an add-on therapy to L-dopa. Xadago is safinamide, which has dopaminergic properties (highly selective and reversible inhibition of monoamine oxidase-B) and also non-dopaminergic properties (selective sodium channel blockade and calcium cahnnel modulation). For more information go to Xadago Safinamide was already available in a lot of European countries. For the news release go to : News release
21st March 2017 - New research
LOSS OF L-DOPA EFFECT IN ADVANCED PARKINSON'S DISEASE
Late-stage Parkinson's Disease is dominated by the loss of autonomy due to motor and non-motor symptoms which can be marginally corrected by medication adjustments. However, controversy exists on the mechanisms underlying the decrease in benefit from L-dopa. So researchers assessed the response to L-dopa in late-stage Parkinson's Disease.
People with late stage Parkinson's Disease and people who had undergone Deep Brain Stimulation underwent an acute L-dopa challenge test. Those people with late stage Parkinson's Disease improved by only 11%, whereas those people who had undergone Deep Brain Stimulation improved by 37%. Rest tremor showed the largest improvement. However, the magnitude of the response to L-dopa was correlated with the severity of dyskinesias in people with late stage Parkinson's Disease.
As the Parkinson's Disease symptoms improved, even though the improvement was mild, the dyskinesia worsened. A decrease in L-dopa response is therefore an indicator of the progression of Parkinson's Disease.
Reference : Parkinsonism and Related Disorders  26 : 10-16 (M.Fabbri, M.Coelho, D.Abreu, L.C.Guedes, M.M.Rosa, N.Costa, A.Antonini, J.J.Ferreira) Complete abstract In order to refer to this article on its own click here
18th February 2017 - New research
VIRTUAL REALITY AIDS PARKINSON'S DISEASE
Virtual reality (VR) technology has been proposed as a new means of rehabilitating people with Parkinson's Disease that has added value over that of physiotherapy. It potentially optimises motor learning in a safe environment, and by replicating real-life scenarios could help improve functional activities of daily living.
Virtual reality (VR) means experiencing things through computers that don't really exist. It is a believable, and interactive 3D computer-created world that you can explore so that you feel you really are there, both mentally and physically. For more information go to : Virtual Reality
Most of the studies intended to improve motor function using commercially available devices were compared with the use of physiotherapy. The interventions lasted for between 4 and 12 weeks. In comparison to physiotherapy, Virtual Reality may lead to a moderate improvement in step and stride length. Virtual Reality and physiotherapy may have similar effects on gait, balance, and quality of life.
However, the authors concluded that there was low-quality evidence of a positive effect of short-term Virtual Reality exercise on step and stride length.
Reference : The Cochrane Database of Systematic Reviews  12 : CD010760 (K.Dock, E.M.Bekkers, V.Van den Bergh, P.Ginis, L.Rochester, J.M.Hausdorff, A.Mirelman, A. Nieuwboer) Complete abstract In order to refer to this article on its own click here
12th February 2017 - News release
L-DOPA INHALER IMPROVES PARKINSON'S DISEASE
The L-dopa inhaler CVT-301 significantly improved Parkinson's Disease symptoms in clinical trials. CVT-301 utilizes ARCUS® for inhaled therapeutics. CVT-301 is designed to deliver a precise dose of a dry powder formulation of L-dopa. Inhaled treatments enter the body through the lungs and then reach the brain far more quickly, by bypassing the digestive system. For more information go to dementia : Arcus
A Phase 3 clinical trial of patients who received CVT-301 in addition to their oral carbidopa/levodopa showed a significant improvement in motor function in people with Parkinson's Disease experiencing OFF periods. Two doses of were assessed - 84 mg and 60 mg (equivalent to 50 mg and 35 mg fine-particle doses). Out of 339 patients, only 6 taking 60mg, and only 2 taking 84mg reported serious adverse effects. The safety profile of CVT-301 was consistent with the Phase IIb clinical trial.
In a previous study the effect of the L-dopa inhaler was around 10 minutes, which is far quicker than the effect of L-dopa when it is taken orally. This would enable the widespread additional use of the L-dopa inhaler for when a quicker effect is required. Acorda said it will file an NDA with the FDA (the U.S. medicines authority) by the end of the second quarter, and a marketing authorisation application with the European Medicines Agency by the end of 2017, pending additional data analyses. News release : News release In order to refer to this article on its own click here
4th February 2017 - New
SECTION 1 HISTORY OF PARKINSON'S DISEASE : Chapter 1 (The history of
Parkinson's Disease - includes descriptions of it in ancient India, ancient
China, the Bible, ancient Greece, ancient Rome, in medieval history, and
during the 16th, 17th, 18th and recent centuries), Chapter 2 (Famous people
with Parkinson's Disease)
APPENDIX : Appendix 1 (Parkinson's Disease organisations), Appendix 2 (Parkinson's Disease web sites), Appendix 3 (Parkinson's Disease nursing books) CLICK HERE FOR MORE DETAILS
26th January 2017 - New research
MILD COGNITIVE IMPAIRMENT IN PARKINSON'S DISEASE
Researchers have examined the incidence, progression, and reversion of mild cognitive impairment in people with Parkinson's Disease (PD-MCI). Mild cognitive impairment (MCI) is an intermediate stage between the cognitive decline of normal ageing and the more-serious decline of dementia. It can involve problems with memory (such as forgetting recent events or repeating the same question), language, thinking, and judgement. For more information go to dementia : Dementia
People with Parkinson's Disease were assessed at diagnosis, after 1 year, after 3 years, and after 5 years. At the outset, 20% of them had PD-MCI, after 1 year 30%, after 3 years 43%, and after 5 years almost half of them (49). Few of those people (7%) who did not have mild cognitive impairment at the outset developed dementia within the next 5 years. Of those that did have mild cognitive impairment at the outset, 39% of them developed dementia within 5 years. Of those that had mild cognitive impairment after 1 year, 59% of them developed dementia within 5 years.
Over 27% of those people with PD-MCI at the outset actually rid their cognitive impairment after 5 years, as did 24% of people who had developed cognitive impairment during the first 5 years. However, they were still far more prone to eventually developing dementia. Although dementia often occurs as Parkinson's Disease worsens, Parkinson's Disease and dementia are biochemically distinct. Dementia is not actually a dopaminergic symptom.
21st January 2017 - New research
SQUALAMINE FOR ALPHA-SYNUCLEIN IN PARKINSON'S DISEASE
Accumulation of alpha-synuclein is associated with Parkinson's Disease and related syndromes. Squalamine was discovered in the tissues of the dogfish shark. For more information go to sqalamine : For more information go to : Squalamine
Squalamine, which is a natural product with known anticancer and antiviral activity, has been found to dramatically affect the aggregation of alpha-synuclein. Researchers assessed the mechanism of action of squalamine by investigating its interaction with lipid vesicles, and found that sqalamine displaces alpha- synuclein from the surfaces of lipid vesicles, thereby blocking the first steps in its aggregation. Squalamine almost completely suppresses the toxicity of alpha-synuclein by inhibiting their interactions with lipid membranes.
Researchers suggest that squalamine could therefore be a means of treating Parkinson's Disease, which is associated with alpha-synuclein.
When L-dopa is formed insufficiently, iron accumulation can occur. Iron accumulation increases the aggregation of alpha-synuclein. Superoxide anion can also be produced. Superoxide anion is broken down to hydrogen peroxide, which can also increase the aggregation of alpha-synuclein. So it is Parkinson's Disease, due to insufficient formation of L-dopa, that causes the aggregation of alpha-synuclein, not alpha-synuclein that causes Parkinson's Disease.
Reference : Proceedings, National Academy of Sciences, USA  Jan 17 [Epub ahead of print] (M.Perni, C.Galvagnion, A.Maltsev, G.Meisl, M.B.Müller, P.K.Challa, J.B. Kirkegaard, P.Flagmeier, S.I.Cohen, R.Cascella, S.W.Chen, R.Limboker, P.Sormanni, et al) Complete abstract In order to refer to this article on its own click here
31st December 2016 - New resrearch
DOUBLED RISK OF BRAIN TUMOR IN PARKINSON'S DISEASE
In Parkinson's Disease there is a decreased risk of cancer, except for melanoma. This study specifically evaluated the risk of brain tumor in Parkinson's Disease. A brain tumour is a growth of cells that multiplies in an uncontrollable way. It can be cancerous (malignant) or non-cancerous (benign). The symptoms can include : severe headaches, seizures, nausea, vomiting and drowsiness, mental or behavioural changes, progressive weakness on one side of the body, vision or speech problems. For more information go to : Brain tumor
This extensive study involved nearly 3000 people with Parkinson's Disease. The risk of developing a brain tumor was found to be significantly higher in people with Parkinson's Disease. The risk of developing a brain tumor was more than doubled. Benign brain tumor exhibited a slightly higher risk. The risk developing a benign brain tumor was even higher in females. An analysis of the age groups found that mostly only those between 50 and 64 years old had a higher risk of developing a brain tumor.
The researchers concluded that people with Parkinson's Disease are at a higher risk of developing a brain tumor but that the exact underlying causes require further investigation.
30th December 2016 - New research
OPICAPONE CLINICAL TRIAL RESULTS FOR PARKINSON'S DISEASE
Catechol O-methyltransferase (COMT) inhibitors are used for end-of-dose motor fluctuations associated with L-dopa therapy in people with Parkinson's Disease. Current COMT inhibitors can cause adverse effects or show moderate improvement. Opicapone, which is intended to overcome these problems, has recently been authorised for sale as Ongentys by the European Commission. For more information go to : Ongentys
The efficacy and safety of opicapone was evaluated when taking daily dosages of 25mg and 50-mg when added to the existing use of L-dopa in people with Parkinson's Disease.
Treatment with a daily 50mg dose of opicapone was associated with a significant reduction in mean daily off-time in people with Parkinson's Disease who were taking L-dopa. The change in off time was a reduction of 64 minutes for those taking a placebo, 101 minutes for those taking 25mg opicapone, and 118 minutes for those people taking 50mg opicapone. The off-time reduction was sustained throughout the study period.
The most common adverse events in those people taking opicapone were dyskinesia, constipation, and dry mouth. Nearly 12% of patients discontinued the study.
Reference : JAMA Neurology  Dec 27 [Epub ahead of print] (A.J.Lees, J.Ferreira, O.Rascol, W.Poewe, J.F.Rocha, M.McCrory, P.Soares-da-Silva) Complete abstract In order to refer to this article on its own click here
30th November 2016 - New research
FIRST ASSESSMENT OF THE ANTI-ALPHA-SYNUCLEIN PRX002 FOR PARKINSON'S DISEASE
Alpha-synuclein can accumulate under certain conditions, primarily in Parkinson's Disease, dementia with Lewy bodies, and multiple system atrophy, but also in Alzheimer's Disease and neuroaxonal dystrophies. Small amounts of alpha-synuclein can also occur in individuals who do not have neurological disorders.
PRX002 is an antibody that targets α-synuclein, which has been shown in preclinical animal studies to reduce α-synuclein pathology and to protect against cognitive and motor deteriorations and progressive neurodegeneration. This first-in-human, phase 1 clinical trial assessed the impact of PRX002 administered to healthy participants in 5 doses (either 0.3, 1, 3, 10, or 30 mg/kg) or a placebo. PRX002 demonstrated favorable safety, tolerability, and pharmacokinetic profiles at all doses tested, with no immunogenicity.
No serious adverse events, discontinuations as a result of adverse events, or dose-limiting toxicities were reported. A significant dose-dependent reduction in free serum α-synuclein was apparent within 1 hour after the administration of PRX002.
Reference : Movement Disorders  Nov 25 [Epub ahead of print] (D.B.Schenk, M.Koller, D.K.Ness, S.G.Griffith, M.Grundman, W.Zago, J.Soto, G.Atiee, S.Ostrowitzki, G.G.Kinney) Complete abstract In order to refer to this article on its own click here
17th November 2016 - New research
HEATWAVES INCREASE MORTALITY IN PARKINSON'S DISEASE
Parkinson's Disease is one of the factors associated with a higher risk of mortality during heat waves. The use of certain neuroleptic drugs to control some of the complications of Parkinson's Disease appears to be what relates Parkinson's Disease to an increase in heat-related mortality. There was a maximum daily temperature of 30°C at which Parkinson's Disease related hospital admissions were at a minimum. However, a temperature of 34°C coincides with a clear increase in the number of hospital admissions.
For people with Parkinson's Disease, for every increase of 1°C above the threshold temperature of 30°C the likelihood of an admission to hospital because of the heat increased.
Reference : Environmental International  89-90 : 1-6 (C.Linares, P.Martinez-Martin, C.Rodríguez-Blázquez, M.J.Forjaz, R.Carmona, J.Díaz) Complete abstract In order to refer to this article on its own click here
12th November 2016 - New research
PEPTOIDS AS A BIOMARKER FOR PARKINSON'S DISEASE
Costly methods of diagnosis such as the SPECT scan or the PET scan are used for the indication of Parkinson's Disease. However, in early Parkinson's Disease a far less costly and relatively non-invasive biomarker would be preferable.
Researchers identified a peptoid called PD2, which binds significantly higher levels of IgG3 antibody in those people with Parkinson's Disease. The PD2 peptoid was found to be 68% accurate in identifying Parkinson's Disease, which is less accurate than existing methods. However, PD2 was 84% accurate in identifying new cases of Parkinson's Disease. It is new cases of Parkinson's Disease that existing methods are not so accurate with. PD2 levels are also positively correlated with the United Parkinson's Disease Rating Scale score, which is the primary symptom questionnaire for Parkinson's Disease. So the researchers concluded that PD2 may be useful for the diagnosis of early Parkinson's Disease.
Reference : NPJ Parkinsons Disease  16012 Epub Jun 23 (U.Yazdani, S.Zaman, L.S.Hynan, L.S.Brown, R.B.Dewey, D.Karp, D.C.German) Complete abstract In order to refer to this article on its own click here
9th November 2016 - New research
CAFFEINE REDUCES PARKINSON'S DISEASE SYMPTOMS
Higher caffeine consumption has been associated with reduced risk of Parkinson's Disease. Besides coffee, caffeine also occurs to a lesser extent in tea, yerba mate, cola drinks, cocoa, and chocolate.
The present study assessed people who were newly diagnosed with Parkinson's Disease over the following four years. Higher caffeine consumption in people with Parkinson's Disease was associated with a lower rate of starting L-dopa treatment, down to 63% of normal. Each additional cup of espresso per day (50 mg of caffeine) was associated with a 5-point lower score on the UPDRS part III (motor symptoms), with a 50% reduction in L-dopa dosage, but was not associated with a lower score on the UPDRS part IV (therapy complications).
Reference : Parkinsonism and Related Disorders  32 : 116-119 (M.Moccia, R.Erro, M.Picillo, C.Vitale, K. Longo, M.Amboni, M.T.Pellecchia, P.Barone) Complete abstract In order to refer to this article on its own click here
8th November 2016 - News report
JANET RENO DIES WITH PARKINSON'S DISEASE
Janet Reno (1938-2016) has died with Parkinson's Disease. She was the first U.S. Attorney General to be a woman. She was nominated to be Attorney General by President Bill Clinton. Janet Reno was the U.S. Attorney General from 1993 until 2001 during the presidency of President Clinton. In 1995, while serving as Attorney General, she announced that she had Parkinson's Disease. In 2002, after ceasing to be the Attorney General, she failed to become the Governor of Florida and retired from public office. She eventually had Parkinson's Disease for over 20 years. She spent her final days at home surrounded by family and friends. She died aged 78 from the "complications" of Parkinson's Disease.
5th November 2016 - New research
PARKINSON'S DISEASE DOUBLES THE RISK OF SUICIDE
Parkinson's Disease has been found to double the risk of suicide. Those factors in people with Parkinson's Disease most associated with suicide are : being male, initial extremity of motor symptom onset, history of depression, delusion, any psychiatric disorder, and higher L-dopa dosage. Other Parkinson's Disease related variables such as Parkinson's Disease symptom score (UPDRS motor score) were not associated with suicide. Dopamine normally stimulates the mesocortical pathway in the brain, which is associated with emotional stimulation. Consequently, insufficient dopamine, which is what occurs in Parkinson's Disease, is associated with emotional depression.
Reference : Parkinsonism and Related Disorders  32 : 102-107 (T.Lee, H.B.Lee, M.H.Ahn, J.Kim, M.S.Kim, S.J.Chung, J.P.Hong) Complete abstract In order to refer to this article on its own click here
4th November 2016 - New research
ANTIOXIDANT VITAMINS AND THE RISK OF PARKINSON'S DISEASE
Oxidative stress is proposed to be one of the potential mechanisms leading to deterioration in Parkinson's Disease. However, previous studies investigating the association between antioxidant vitamins, such as vitamins C, E and A (carotenoids), and the risk of Parkinson's Disease have produced inconsistent results.
Over 1000 people with Parkinson's Disease were assessed concerning the effect of antioxidant vitamins on Parkinson's Disease. Dietary intakes of vitamin E and vitamin A (carotenoids) were not associated with the risk of Parkinson's Disease. However, dietary vitamin C intake was significantly associated with a reduced risk of Parkinson's Disease, down to 80%, but this was not long term. For vitamins E and C, intake from foods and supplements combined were also unrelated to Parkinson's Disease risk..
In Parkinson's Disease L-dopa is not formed properly. Superoxide anion can be formed when L-dopa is not formed properly. Superoxide anion is broken down by the enzymes superoxide dismutase and catalase, which require Vitamin C and Vitamin E. In previous studies the greatest effect of antioxidants was with the use of Vitamin C and Vitamin E, which were shown to slow down the progression of Parkinson's Disease.In Parkinson's Disease L-dopa is not formed properly. Superoxide anion can be formed when L-dopa is not formed properly. Superoxide anion is broken down by the enzymes superoxide dismutase and catalase, which require Vitamin C and Vitamin E. In previous studies the greatest effect of antioxidants was with the use of Vitamin C and Vitamin E, which were shown to slow down the progression of Parkinson's Disease.
Reference : Movement Disorders  Oct 27 [Epub ahead of print] (K.C.Hughes, X.Gao, I.Y.Kim, E.B.Rimm, M.Wang, M.G.Weisskopf, M.A.Schwarzschild, A.Ascherio) Complete abstract In order to refer to this article on its own click here
28th October 2016 - New research
AIR POLLUTION INCREASES THE RISK OF PARKINSON'S DISEASE
Nitrogen dioxide is a chemical compound with the formula NO2. Nitrogen dioxide is an intermediate in the industrial synthesis of nitric acid, millions of tons of which are produced each year. At higher temperatures it is a reddish-brown gas that has a characteristic sharp, biting odour and is a prominent air pollutant. Air pollution, especially as nitrogen dioxide, has been found to increase the risk of developing Parkinson's Disease.
High exposure to nitrogen dioxide, largely because of pollution, trebled the risk of Parkinson's Disease. Another study suggests that ambient air pollution exposure, especially from traffic-related pollutants such as nitrogen dioxide and carbon monoxide also increases the risk of Parkinson's Disease. Previous studies have shown that lower exposures to nitrogen dioxide in air pollution did not significantly increase the risk of Parkinson's Disease.
Nitrogen dioxide toxicity causes the nitration of the tyrosine residues of tyrosine hydroxylase. Tyrosine hydroxylase is the enzyme that produces L-dopa and eventually dopamine. It is by this means that nitrogen dioxide has its adverse effects.
References : Environmental Research  151 : 713-720 (P.C.Lee, O. Raaschou-Nielsen, C.M.Lill, L.Bertram, J.S.Sinsheimer, J.Hansen, B. Ritz), Complete abstract
22nd October 2016 - New research
L-DOPA INHALER FOR PARKINSON'S DISEASE
CVT-301 is the name of an inhaled version of L-dopa presently being developed for the treatment of Parkinson's Disease. CVT-301 uses the ARCUS inhalation technology, which delivers a reliable and consistent drug dose with a compact, breath actuated inhaler. It uses a dry powder and inhaler combination that is unique in its ability to deliver a large, precise dose independent of inspiratory flow rate from a simple, easy-to-use device suitable for convenient self-administration.
Among people with Parkinson's Disease inhaling CVT-301 as a single 50mg dose during an "off" period, 77% of them showed an increase in plasma L-dopa within 10 minutes.
Only 27% of people with Parkinson's Disease taking oral carbidopa/levodopa reached the same levels. The improvements in motor function were seen as quickly as 5 and 15 minutes after administration, which were the earliest assessment times. So the effect may have been even quicker. The most common adverse effect was a cough. All cough events were mild to moderate, occurred at the time of inhalation, resolved rapidly, and became less frequent after initial dosing. Less common adverse effects were dizziness and headache. There were no adverse effects on cardiovascular or lung function.
The speed of effect of the L-dopa inhaler and its limited adverse effects could enable it to be widely used when a rapid effect on Parkinson's Disease is required.
26th September 2016 - New research
NEWLY DISCOVERED GENETIC CAUSE OF PARKINSON'S DISEASE
A new genetic cause of Parkinson's Disease has been discovered called TMEM230. A small proportion of cases of Parkinson's Disease have a genetic cause. Most genetic causes make Parkinson's Disease more likely rather than inevitable. Having relatives with Parkinson's Disease does not mean that it has been inherited. People can have the same medical disorder due to similar environmental factors that have led to them having Parkinson's Disease.
The newly discovered genetic disorder, TMEM230, is located on the short arm of chromosome 20 (20pter-p12). Genetic disorders normally occur due to inheritance, either from both parents (autosomal recessive), or from one parent (autosomal dominant). TMEM230 is autosomal dominant (from one parent). The function of TMEM230 is to produce vesicles involved in packaging the neurotransmitter dopamine in the dopaminergic neurons and then secreting it. It is insufficient dopamine that causes Parkinson's Disease. The clinical features of TMEM230 are typical of Parkinson's Disease. TMEM230 was found in people with Parkinson's Disease from both North America and Asia, including China.
There are now 39 known genetic causes of Parkinson's Disease. The most prominent of these are given a PARK number (from PARK 1 to PARK 23), with some of the well known being : PARK 1 (Alpha-Synuclein), PARK 2 (Parkin), PARK 3 (Lewy body), PARK 5 (UCHL1), PARK 6 (Pink 1), PARK 7 (DJ-1), and PARK 8 (LRRK2). Of the more than a dozen genetic causes without a PARK number include Tyrosine Hydroxylase, and Dopa decarboxylase, which can cause Parkinson's Disease from birth.
Reference : Nature Genetics  48 (7) : 733-739 (H.X.Deng, Y.Shi, Y.Yang, K.B. Ahmeti, N.Miller, C.Huang, L.Cheng, H.Zhai, S.Deng, K.Nuytemans, N.J.Corbett, M.J.Kim, H.Deng, B.Tang, Z.Yang, Y.Xu, P.Chan, B.Huang, X.P.Gao, Z.Song, et al) Complete abstract In order to refer to this article on its own click here
19th September 2016 - New research
PRELADENANT FAILS PARKINSON'S DISEASE CLINICAL TRIALS
Preladenant, an adenosine 2A antagonist, has been assessed for its effect on daily OFF time when administered to people who have Parkinson's Disease who were taking L-dopa. The main drugs for Parkinson's Disease are dopaminergic (they aim to increase the activity of dopamine). Adenosine antagonists instead affect the adenosine receptors. Those adenosine antagonists that are presently being assessed for their use in the treatment of Parkinson's Disease include tozadenant, preladenant, istradefylline and caffeine.
People who have Parkinson's Disease who were taking L-dopa were given 2mg, 5mg or 10mg preladenant for 12 weeks. each dosage was taken by over 100 patients. The primary measure was the decrease in off time. In contrast to previous clinical trials, preladenant in this study did not demonstrate statistically significant efficacy. The primary outcome were reductions in off time of 42 minutes for 2mg, 30 minutes for 5mg, and 18 minutes for 10mg preladenant. Overall, preladenant was well tolerated, and the frequency of adverse effects appeared to be dose related.
In this phase 2 clinical trial, preladenant used as adjunctive therapy in people on stable doses of L-dopa did not sufficiently reduce the mean OFF time.
Reference : Parkinsonism & Related Disorders  Aug 27 [Epub ahead of print] (N.Hattori, M.Kikuchi, N.Adachi, D.Hewitt, S.Huyck, T.Saito) Complete abstract In order to refer to this article on its own click here
27th August 2016 - New research
SMALL AND LARGE FIBER NEUROPATHY IN PARKINSON'S DISEASE
Recent studies have reported that peripheral neuropathy is common in people with Parkinson's Disease and raised the possibility that L-dopa neurotoxicity is the main culprit. Peripheral neuropathy develops when nerves in the body's extremities, such as the hands, feet and arms, are damaged. This can cause numbness and tingling in the feet or hands, burning pain in affected areas, and muscle weakness, especially in the feet. For more information go to : Neuropathy
In people with Parkinson's Disease, neuropathy screening was carried out, including neurological examination, nerve conduction studies and skin wrinkling tests. Two of the tests showed that 57% and 42% of people with Parkinson's Disease had abnormal results that indicated polyneuropathy. The prevalence in people with a Parkinsonism was similar to people with Parkinson's Disease but the results were less severe. The results showed that polyneuropathy was more common in Parkinson's Disease than previously assumed, but the cause was not solely attributed to taking L-dopa.
The researchers concluded that large fiber and small fiber polyneuropathy are common in people with Parkinson's Disease. However, instead of concluding that the cause was L-dopa, the cause of the neuropathy was thought to be multifactorial. Neuropathy was previously related to age, vitamin B12 deficiency, serum folate levels, and especially L-dopa use.
Reference : BMC Neurology  16 : 139 (D.F.de Araújo, A.P.de Melo Neto, I.S. Oliveira, B.S.Brito, I.T.de Araújo, I.S.Barros, J.W.Lima, W.G.Horta, FdeA.Gondim) Complete abstract In order to refer to this article on its own click here
21st August 2016 - New research
NASAL GEL MAGNIFIES PARKINSON'S DISEASE DRUG EFFECTS
A nasal gel has been developed that can greatly increase the bioavailability of ropinirole. Ropinirole (Requip), which is a dopamine agonist for the treatment of Parkinson's Disease, normally has low bioavailability when it is taken orally. For more information go to : Ropinirole
Thermoreversible nasal gels were prepared and formulations were evaluated for various parameters such as gelling time, gelling temperature, gel strength, adhesive force, diffusion, and bioavailability. Formulations displayed gelling at nasal temperature and the time was found to be less than the time taken to clear the gel. The time the gel spent nasally increased due to mucoadhesion and increased gel strength. Nasal gel formulations showed drug release between 56% and 100% within 5 hours. The gel had a protective effect on the mucosa unlike plain ropinirole which showed evidence of moderate cellular damage.
The bioavailability of ropinirole in the brain was increased by five times when administered nasally using the gel when compared to intravenous administration. Thermoreversible nasal gel was consequently found to be a promising means of increased drug delivery for Parkinson's Disease.
Reference : Drug Development and Industrial Pharmacy  Aug 17 : 1-34 [Epub ahead of print] (M.Rao, D.K.Agrawal, C.Shirsath) Complete abstract In order to refer to this article on its own click here
31st July 2016 - News release
CANCER DRUG NILOTINIB ASSESSED FOR PARKINSON'S DISEASE
The Michael J.Fox Foundation is assessing the clinical use and development of the cancer drug nilotinib for treating Parkinson's Disease by carrying out a full scale clinical trial. Nilotinib is a drug approved for chronic myelogenous leukemia, a cancer of the white blood cells, under the brand name Tasigna. For more information go to the : Michael J.Fox Foundation
Previous studies have concerned the possible use of nilotinib and Parkinson's Disease. Their findings are summarised here. Nilotinib is a cAbl tyrosine kinase inhibitor that is normally used for the treatment of cancer. It is claimed to facilitate the degradation of alpha-synuclein. Efficacy has only been assessed concerning motor function in animals that did not have Parkinson's Disease. Doses of 150mg or 300mg for 6 months were claimed to be safe and well tolerated despite side effects. For more details of the previous studies concerning nilotinib and Parkinson's Disease go to : Nilotinib studies
Although alpha-synuclein is often claimed to cause and indicate Parkinson's Disease, alph-synuclein accumulates in a variety of neurological conditions and in people who do not have neurological disorders. Therefore, an accumulation of alpha-synuclein does not indicate that somebody has Parkinson's Disease. In Parkinson's Disease, the faulty formation of L-dopa causes the formation of the superoxide anion, which causes the aggregation of alpha-synuclein. So instead of alpha-synuclein accumulation being the cause of Parkinson's Disease, Parkinson's Disease causes an accumulation of alpha-synuclein. In order to refer to this article on its own click here
30th July 2016 - New novel
SAY THAT AGAIN
Publisher's description : Benedict Marshall is a charismatic, articulate, award winning playwright. At 62, his life is alteredPublisher's description : Benedict Marshall is a charismatic, articulate, award winning playwright. At 62, his life is altered in one week by two events - being diagnosed with Parkinson’s Disease and meeting Nell, a much younger, out of work actress.
They form an instant and unlikely close friendship. He shares his guilt and introspection about his past and the fear and isolation he feels in his own body with Nell and she confides in him the insecurities and challenges she faces in her profession. Benedict valiantly battles against his Parkinson’s Disease with black humour and charm, while trying to deny to his family and himself, his unspoken love for the young woman who everyone warns him can only be after his money. Click here for more details For more books concerning Parkinson's Disease go to Parkinson's Disease books
20th July 2016 - New research
ULTRASOUND ELASTOGRAPHY - MEANS OF ASSESSING RIGIDITY IN PARKINSON'S DISEASE
Ultrasound elastography is a means of assessing the mechanical properties of tissue, by applying stress and detecting tissue displacement using ultrasound. It provides information on tissue stiffness. For more information go to : Ultrasound Elastography
Ultrasound shear wave elastography has been used to assess muscle stiffness in people with Parkinson's Disease. The assessments were made by assessing the biceps of people with Parkinson's Disease.Around Ultrasound shear wave elastography of the longitudinal biceps brachii was performed on 46 people with Parkinson's Disease and 31 healthy controls The mean Young's modulus was 59 kPa in remarkably symptomatic arms, 47 kPa in mildly symptomatic arms, and 24 kPa in healthy controls.
A significant difference was found between healthy controls and all people with Parkinson's Disease. The distinctiveness of the results enable Ultrasound shear wave elastography to be used as a quantitative assessment of muscle stiffness in people with Parkinson's Disease..
Reference : Clinical Imaging  40 (6) : 1075-1080 (L.J.Du, W.He, L.G. Cheng, S.Li, Y.S.Pan, J.Gao)Complete abstract In order to refer to this article on its own click here
16th July 2016 - News release
ONGENTYS - NEW COMT INHIBITOR FOR PARKINSON'S DISEASE
The European Commission has approved Ongentys (opicapone) for use alongside preparations of L-dopa and dopa decarboxylase inhibitors (such as Sinemet and Madopar) in people with Parkinson's Disease who have end-of-dose motor fluctuations, and who cannot be stabilised on those combinations. Opicapone is a new COMT inhibitor. COMT inhibitors aim to maintain dopamine levels for longer.
Two studies were carried out on people with Parkinson's Disease. In the first study, off periods were shortened by 117 minutes (nearly 2 hours) by taking Ongentys 50 mg, compared with 96 minutes (over 1 and a half hours) by taking the COMT inhibitor entacapone, and 56 minutes (less than 1 hour) by taking a placebo. In the second study, off periods were shortened by 119 minutes using Ongentys 50 mg, compared with 64 minutes in patients taking placebo. Therefore, Ongentys was found to be more effective than entacapone, which is presently the most widely used COMT inhibitor.
The most common adverse effects are disorders of the nervous system (brain and spinal cord). Among these, dyskinesia may affect around 2 in 10 people.
10th July 2016 - New research
A POTENTIAL CASE OF REMISSION OF PARKINSON'S DISEASE
Researchers have presented the case of a 78-year-old male who, 16 years ago, was diagnosed with Parkinson's Disease by a neurologist. The patient initially presented with left-hand tremor, stooped posture, shuffling gait, and frequent falls, which eventually progressed to bilateral motor symptoms after 3 years.
However, since 2012, his symptoms and signs have almost completely remitted, and he has been off all pharmacotherapy for that time. The accuracy of the initial Parkinson's Disease diagnosis is supported by : an appropriate clinical presentation, history of positive response to Sinemet, and an abnormal SPECT DaT scan. This case therefore suggests the possibility of the remission of symptoms in some patients. The authors propose that the patient's long history of meditation may have been one of the contributing factors of his improvement because meditation has been shown to release dopamine. Parkinson's Disease is primarily due to insufficient dopamine.
There is a tendency for Parkinson's Disease symptoms to get gradually and progressively worse. However, dopamine levels, even in Parkinson's Disease, fluctuate continuously. There is therefore no reason why dopamine levels and therefore Parksinson's Disease can not improve.
Reference : Journal of Complementary Integrative Medicine  [Epub ahead of print] (K.Smart, R.Durso, J.Morgan, P.McNamara)Complete abstract In order to refer to this article on its own click here
16th June 2016 - New research
MIRROR MOVEMENTS IN PARKINSON'S DISEASE
Over 95% of people with Parkinson's Disease have been found to experience mirror movement. Mirror movement is a condition in which intentional movements of one side of the body are mirrored by involuntary movements of the other side. For example, when an affected individual makes a fist with the right hand, the left hand makes a similar movement. Mirror movements mainly involve upper limbs, especially the hands and fingers. For more information go to : Mirror movements
Around 90% or more of people with Parkinson's Disease exhibit mirror movements. Mirror movements are often reported in early Parkinson's Disease. There is a trend towards mirror movements when the symptoms of Parkinson's Disease are less severe not more severe. Mirror movements are usually a clinical feature of the unaffected or less affected side in mild Parkinson's Disease. A previous study found that mirror movements were actually less common in people with Parkinson's Disease.
Mirror movements reflect an abnormal enhancement of the "physiological mirroring" that can be observed in normal circumstances during complex and effortful tasks. It was hypothesized that, in Parkinson's Disease, enhanced mirroring is caused by a failure of basal ganglia output to support the cortical network that is responsible for the execution of strictly unimanual movements. Expression of overt mirror movement may be due to the combination of enhanced motor cortex excitability and an earlier onset of activation in the mirror hand.
Reference : Journal of Neurological Science  366 : 171-176 (P. Chatterjee, R.Banerjee, S.Choudhury, B.Mondal, M.U.Kulsum, K. Chatterjee, H.Kumar) Complete abstract In order to refer to this article on its own click here
8th June 2016 - New book
EVERYTHING YOU NEED TO KNOW ABOUT CAREGIVING FOR PARKINSON'S DISEASE
Publisher's description : This comprehensive guide answers your most important questions about caring for someone with Parkinson's Disease. Written in easy to understand every day English, this book is the result of 25 years experience and research in living a life with Parkinson's Disease. Filled with information, tips and helpful hints on a wide range of topics, Caregiving for Parkinson’s will help guide you through all the many stages of caregiving. Inspired by her mom who has lived with and battled the disease for 25 years, author Lianna Marie wrote this book and founded the website AllAboutParkinsons.com.
The website has had over one million visitors and the book has been sold in 47 countries worldwide. Click here for more details For more books concerning Parkinson's Disease go to Parkinson's Disease books
3rd June 2016 - News report
MUHAMMAD ALI HAS DIED WITH PARKINSON'S DISEASE
Muhammad Ali (1942-2016), the three time World Heavyweight boxing champion, has died with Parkinson's Disease. He was hospitalized on 2nd June 2016 with a respiratory condition. His condition was initially described as fair. However, the following day his condition worsened and he was placed on life support. His condition did not improve. Late on 3rd June 2016 it was announced that Muhammad Ali had died at the age of 74. A funeral will be held in his hometown of Louisville, Kentucky.
Muhammad Ali became Olympic champion in 1960 at the Rome Olympics. In 1964 he became the youngest world heavyweight champion by beating Sonny Liston. In 1967, he was stripped of his world heavyweight title for refusing to be drafted into the U.S. Army, because of his conscientious objections. He was allowed to resume boxing again in 1970. In 1974 he regained the world heavyweight title by beating George Foreman, and retained it the following year against Joe Frazier. In 1978 he lost the title to Leon Spinks but regained it the same year before relinquishing the title.
He was diagnosed with Parkinson's Syndrome in 1984 at the age of 42. In 1996, with very apparent Parkinsonian symptoms, he lit the flame at the Summer Olympics in Atlanta. In 1997 he set up The Muhammad Ali Parkinson Center to help people with Parkinson's Disease. In 2012, he was a bearer of the Olympic Flag during the opening ceremonies of the 2012 Summer Olympics in London. He was helped to his feet to stand before the flag due to the deterioration of his Parkinson's Disease. After further deteriorations in his health over the next few years he died at the age of 74. In order to refer to this article on its own click here
31st May 2016 - New book
NetCE, Mark Rose
Publisher's description : The purpose of this course is to provide needed information about the assessment and treatment of Parkinson disease so healthcare professionals may implement the necessary interventions appropriately. In addition, members of the public may use this course to enhance their personal knowledge of the subject matter presented. This book emphasizes treatment options for Parkinson's disease, critically assessing pharmacologic and surgical interventions for all aspects of the disease. Evidence from randomized controlled clinical trials is highlighted to develop practical recommendations for clinical practice.
24th May 2016 - New research
THE INCIDENCE OF PARKINSON'S DISEASE IS FALLING
Instead of Parkinson's Disease becoming progressively more common as was assumed, the incidence of Parkinson's Disease, which is the rate at which people are newly diagnosed, has been found to be continuously declining.
The incidence of Parkinson's disease and Parkinsonism were assessed by comparing data from 1990 until 2010, at 1990, 2000 and 2010. All factors were accounted for. The incidence of Parkinson's Disease in 2000 was found to be only 55% of what it was in 1990. The incidence of Parkinson's Disease in 2010 was found to be only 39% of what it was in 1990. The findings showed that the incidence of Parkinsonism in general, and of Parkinson's Disease in particular, decreased substantially between 1990 and 2011, and is continuously declining.
These findings can not indicate that the methods of treating Parkinson's Disease and Parkinsonism have improved because there was already a substantial decline at the point of diagnosis.
Reference : American Journal of Epidemiology  Apr 29 [Epub ahead of print] (S.K. Darweesh, P.J. Koudstaal, B.H.Stricker, A.Hofman, M.A.Ikram) Complete abstract In order to refer to this article on its own click here
19th May 2016 - New research
PHYSICAL ACTIVITY HALVES THE RISK OF PARKINSON'S DISEASE
Regular exercise is known to alleviate the muscular symptoms of Parkinson's Disease. However, it remained unclear as to whether a physically active lifestyle could also reduce the risk of Parkinson's Disease. An assessment was made of (1) overall physical activity over 4 age periods, (2) competitive sports, and (3) occupational physical activity.
The risk of Parkinson's Disease was lower when comparing moderate to vigorous activities to low physical activity in the age range 18-24 years, and even moreso in the age range 45-64, but not in the age range 25-44. People who had consistently engaged in overall physical activity at high levels, before they were 65, had only half the risk of developing Parkinson's Disease when compared to those people with low levels of physical activity. Having participated in competitive sports prior to the age of 25 nearly halved the risk of Parkinson's Disease, down to a 53% chance of developing Parkinson's Disease. Occupational physical activity did not lessen the risk at all.
Exercise or activity of the muscles cause a contraction of the muscles used. The after effect of muscle contraction is reduced muscle contraction. Given that the muscular symptoms of Parkinson's Disease are due to excessive muscle contraction, the subsequent reduction of muscles contraction after exercise lessens the muscular symptoms of Parkinson's Disease. Exercise or activity of the muscles do not increase low dopamine levels, which is the primary cause of Parkinson's Disease.
6th May 2016 - New research
BRADYPHRENIA IN PARKINSON'S DISEASE
Bradyphrenia is mental slowness. Bradyphrenia can consist of slowness of thought, impaired attention and motivation, lack of spontaneity, and inflexibility. Bradyphrenia was well known to occur in Parkinson's Disease. For the first time researchers have assessed how prevalent bradyphrenia is in Parkinson's Disease and what causes it.
Bradyphrenia was found to occur in as many as half of people with Parkinson's Disease. Between 11% and 51% of people with Parkinson's Disease were found to exhibit mental slowness by performing significantly worse on neuro- psychological tests including tests of attention and executive function. However, bradyphrenia was found to be uncommon in people with Parkinson's Disease who did not also have dementia or depression. The results suggest that the depression or dementia that often accompanies Parkinson's Disease is the cause of the bradyphrenia.
Bradyphrenia in Parkinson's disease may also reflect advancing age because the effects of age may be greater in some cases than the effects of basal ganglia disease once motor dysfunction has been allowed for. However, he dopamine system through the medial forebrain bundle projecting from the ventral tegmental area to the nucleus accumbens, ventral striatum (limbic striatum) and the cortex is associated with bradyphrenia.
Reference : Journal of Clinical and Experimental Neuropsychology  May 1 : 1-9 [Epub ahead of print] (T.T.Vlagsma, J.Koerts, O.Tucha, H.T.Dijkstra, A.A.Duits, T.van Laar, J.M.Spikman) Complete abstract In order to refer to this article on its own click here
29th April 2016 - New book
PARKINSON'S DISEASE : CURRENT AND FUTURE THERAPEUTICS AND CLINICAL TRIALS
Nestor Galvez-Jimenez, Hubert H.Fernandez, Alberto J.Espay, Susan H.Fox
Publisher's description : This book emphasizes treatment options for Parkinson's disease, critically assessing pharmacologic and surgical interventions for all aspects of the disease. Evidence from randomized controlled clinical trials is highlighted to develop practical recommendations for clinical practice. Lessons learnt from clinical trials are all addressed. Readers will find the necessary clinical and scientific foundations for the understanding of the disease, the underpinnings of the pathological processes, the identification of disease biomarkers, and the basis for solid therapeutics. The chapters are authored by an international team of specialists in each subject. Click here for more details For more books concerning Parkinson's Disease go to Parkinson's Disease books
25th April 2016 - New research
"EARLY MORNING OFF" IN PARKINSON'S DISEASE
Early Morning Off (EMO) is a lengthy delay in the therapeutic effect of the initial dose of an oral medication in the morning. Early Morning Off (EMO) is a symptom experienced by people at every stage of Parkinson's Disease. However, few studies have assessed how common it is, leaving the extent of its impact almost completely unknown. For a graph showing the effects of EMO go to : Early Morning Off
EMO occurs as there is a delay in the effect of the initial dose of oral medication, possibly due to gastroparesis. Gastroparesis is a chronic condition in which the stomach cannot empty itself in the normal way. For more information go to : Gastroparesis
The analysis assessed the responses from 2205 completed surveys. People with Parkinson's Disease who felt they had EMO amounted to around 80%, with 37% of them stating that EMO was a daily occurrence. The prevalence of EMO increased as Parkinson's Disease worsened. However, even 52% of people with early Parkinson's Disease had EMO. The Quality of Life of those with EMO was also significantly reduced and the odds of caregivers feeling a sense of burden was higher. The prevalence of EMO in the survey results was high, and significantly lowered the persons Quality of Life. EMO was also observed in the early stages of Parkinson's Disease.
Reference : Reference : Journal of Neurological Science  364 : 1-5 (R.Onozawa, J.Tsugawa, Y.Tsuboi, J.Fukae, T.Mishima, S.Fujioka) Complete abstract In order to refer to this article on its own click here
21st April 2016 - New research
ALEXITHYMIA IN PARKINSON'S DISEASE
Alexithymia has been found to be highly prevalent in Parkinson's Disease to the extent that it is commonly part of it. Alexithymia is a personality trait characterised by difficulties identifying and describing feelings and a reduced tendency to think about emotions. For more information go to : Alexithymia
An extensive assessment of the medical databases was carried out. Ten studies reported that alexithymia prevalence was about double in Parkinson's Disease. In previous studies about 20% to 50% of people with Parkinson's Disease have alexithymia, which is about 2 to 4 times normal. Specific dimensions of alexithymia might be related to depression, anxiety, apathy and impulsivity. Two studies on neurological features reported a link between alexithymia and the stage of Parkinsons' Disease. The remaining studies found that alexithymia was independent from neurological symptoms and dopaminergic therapy.
There is a strong association between alexithymia and the severity of depression, which appears to be the primary cause. The results suggest that alexithymia is a primary characteristic of Parkinson's Disease that is often related to depression.
Reference : Parkinsonism and Related Disorders  Mar 30 [Epub ahead of print] (F.Assogna, L.Cravello, M.D.Orfei, N.Cellupica, C.Caltagirone, G.Spalletta) Complete abstract In order to refer to this article on its own click here
11th April 2016 - New research
ADAPTIVE DEEP BRAIN STIMULATION FOR PARKINSON'S DISEASE
Conventional Deep Brain Stimulation is set by a movement disorders specialist and left running continuously without change until the next clinic visit. However, this continuous high voltage stimulation may interfere with normal functioning. In contrast, Adaptive deep brain stimulation (aDBS) has the potential to greatly improve the treatment of Parkinson's disease by optimizing deep brain stimulation in real time according to fluctuating disease and medication state. For more information go to : Adaptive Deep Brain Stimulation
An external portable aDBS system prototype was developed that was designed for clinical testing in people with Parkinson's Disease who had externalised DBS electrodes. The aDBS system was validated by testing both its sensing and stimulation capabilities, and then by testing it in vivo, focusing on the sensing capabilities. By applying the aDBS system prototype in a patient with Parkinson's Disease, evidence was provided that it can track L-dopa and DBS-induced LFP spectral power changes among different patient's clinical states.
Compared to conventional deep brain stimulation (DBS) for people with Parkinson's Disease (PD), the newer approach of adaptive DBS (aDBS), regulating stimulation on the basis of the patient's clinical state, promises to achieve better clinical outcomes, avoid adverse-effects and save time for tuning parameters.
6th April 2016 - New research
THE EMOTIONAL EFFECTS OF DBS ON PARKINSON'S DISEASE
Researchers assessed the effect of Deep Brain Stimulation (DBS) on anxiety, depression and psychosis. Deep Brain Stimulation involves the use of electrodes that are implanted into the brain and connected to a small electrical device that can be externally programmed. DBS can reduce the need for L-dopa and related drugs, which in turn decreases the dyskinesias that are a common side effect of L-dopa. DBS helps to alleviate fluctuations of symptoms and reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device. For more information go to : Deep Brain Stimulation
Improvement of depression and anxiety was apparent after DBS, and was more pronounced in the short-term, an effect that seems to decline in later assessments. Concerning depression, DBS was more effective than medical treatment. However, with anxiety, medical treatments were found to be more effective than DBS. The pattern and course of depression and anxiety following DBS is not clear, although both seem to improve in the short-term. The risk of psychosis remains fairly constant throughout the first five years after DBS implantation.
Results suggest that most psychoses occurring postoperatively are independent of DBS implantation and stimulation settings.
References : Acta Medica Portuguesa  27 (3) : 372-382 (M.I.Couto, A.Monteiro, A.Oliveira, N.Lunet, J.Massano) Complete abstract Neurosurgical Focus  38 (6) : E5 (A.A.Qureshi, J.J.Cheng, A.N.Sunshine, A.Wu, G.M.Pontone, N.Cascella, F.A.Lenz, S.E.Grill, W.S.Anderson) Complete abstract In order to refer to this article on its own click here