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.
18th November 2017 - News report
JESSE JACKSON DIAGNOSED WITH PARKINSON'S DISEASE
Civil rights activist Reverand Jesse Jackson said that he has been diagnosed with Parkinson's Disease. He wrote in a statement that, "My family and I began to notice changes about three years ago. After a battery of tests, my physicians identified the issue as Parkinson's disease, a disease that bested my father." Jesse Jackson added that, "recognition of the effects of this disease on me has been painful." He also said he sees his diagnosis as "a signal that I must make lifestyle changes and dedicate myself to physical therapy in hopes of slowing the disease's progression." The 76-year-old former congressman is a two-time Democratic presidential candidate. The highlight of his career includes participating in civil rights demonstrations with the Reverand Martin Luther King Jr.. For more information go to the news report : News report
28th October 2017 - New research
THE EFFECT OF MEDICAL CANNABIS ON PARKINSON'S DISEASE
Medical cannabis or medical marijuana, are cannabis or marijuana that is recommended by doctors for their patients. It has been claimed to be beneficial for people with Parkinson's Disease. However, its use is controversial, because support for its benefits is based on small clinical studies. For more information go to : Medical cannabis
The duration of medical cannabis use was an average of 19 months (between 2 and 36 months). The average daily dose was 0.9g per day. The delivery of medical cannabis was mainly by smoking cigarettes (in 80% of cases). The size of the effect from the greatest effect to the least effect were for reducing falls 0.89, pain relief 0.73, tremor 0.64, depression 0.64, muscle stiffness 0.62, and then sleep 0.60. The most frequently reported adverse effects from medical cannabis were cough (35%) in those who used medical cannabis by smoking it, and confusion and hallucinations, which were each reported in 17% of people, causing 10% of patients to stop taking cannabis.
Reference : Clinical Neuropharmacology  Oct 20 [Epub ahead of print] (Y.Balash, L.Bar-Lev Schleider, A.D.Korczyn, H.Shabtai, J.Knaani, A.Rosenberg, Y.Baruch, R. Djaldetti, N.Giladi, T.Gurevich) Complete abstract In order to refer to this article on its own click here
23rd October 2017 - New research
PASSIVE SMOKING INCREASES THE RISK OF PARKINSON'S DISEASE
Tobacco smoking is consistently associated with a reduced likelihood of Parkinson's Disease in men and women. So passive smokers were assessed to see whether they were affected in the same way.
Exposure to passive smoke in social settings was positively associated with Parkinson's Disease, increasing the likelihood of developing Parkinson's Disease by 62%. Neither the increasing years of passive smoke exposure, nor the smokiness of the setting affected the likelihood of Parkinson's Disease.
However, household exposure during adulthood was associated with a reduced risk of Parkinson's Disease down to 59% of what would be expected. Household exposure during childhood was not associated with any alteration in the risk of Parkinson's Disease. Workplace exposure was also not associated with the risk of Parkinson's Disease. Among lifelong non-smokers, passive smoke exposure combined across all settings and accumulated over a lifetime was only marginally associated with an increased risk of Parkinson's Disease.
Reference : Parkinsonism and Related Disorders  Oct 4 [Epub ahead of print] (N.M. Gatto, D.Deapen, Y.Bordelon, S.Marshall, L.Bernstein, B.Ritz) Complete abstract In order to refer to this article on its own click here
18th October 2017 - New research
DRIVING SAFETY DECLINES IN PARKINSON'S DISEASE
People with Parkinson's Disease have been assumed to decline in their driving ability due to the problems that Parkinson's Disease causes. People with Parkinson's Disease were assessed in their driving ability and again two years later.
Drivers with Parkinson's Disease performed worse on visual, cognitive, and motor tests, and committed more road safety errors compared to those people who did not have Parkinson's Disease. However, the difference was not as great as expected. The number of errors was about 25% greater with drivers who had Parkinson's Disease and so would not suggest any need for most people with Parkinson's Disease to initially cease driving due to the errors they made. When the tests were repeated those people with Parkinson's Disease performed similarly to those people who did not have Parkinson's Disease.
However, two years later, people with Parkinson's Disease showed greater cognitive decline and worse visual acuity. They had a greater increase in driving errors, with an increase in errors over 4 times that of people who did not have Parkinson's Disease. So it appears that initially although driving ability does not greatly worsen in people with Parkinson's Disease, that driving ability gradually worsens over time.
30th September 2017 - New research
ALPHA-SYNUCLEIN PREDICTS THE COGNITIVE DECLINE IN PARKINSON'S DISEASE
It is often claimed that alpha-synculein is a hallmark of Parkinson's Disease or indicates its severity. It has even been wrongly claimed to be the primary cause of Parkinson's Disease. However, it has instead been found to be related to the cognitive decline that can occur in Parkinson's Disease, especially as Parkinson's Disease worsens.
levels of alpha-synuclein were much higher in people with Parkinson's
Disease. However, although there was a significant increase in plasma
alpha-synuclein levels in people with Parkinson's Disease, in later stages of
Parkinson's Disease there was no correlation with motor symptom severity, as
assessed by Unified Parkinson's Disease Rating Scale part III scores (the
main Parkinson's Disease symptom score). However, plasma alpha-synuclein
levels were significantly higher in people with Parkinson's Disease who had
dementia than in people with Parkinson's Disease who only had mild cognitive
impairment or normal cognition.
The results suggest that plasma alpha-synuclein level correlates with cognitive decline but not with motor severity in people with Parkinson's Disease. Plasma alpha-synuclein could therefore serve as a biomarker for people with Parkinson's Disead at risk of cognitive decline.
Reference : Journal of Neurology, Neurosurgery and Psychiatry  88 (10) : 818-824 (C.H.Lin, S.Y.Yang, H.E.Horng, C.C.Yang, J.J.Chieh, H.H.Chen, B.H.Liu, M.J.Chiu) Complete abstract In order to refer to this article on its own click here
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.