E-MAIL NOTIFICATION : If you want to be notified by e-mail when new articles are added to Parkinson's Disease News, please e-mail [email protected] with the message "subscribe".  No form of identity is required.  E-mail addresses are not used for any other purpose.

THE COMPREHENSIVE GUIDE TO PARKINSON'S DISEASE Keith Bridgeman, Tahira Arsham The Comprehensive Guide to Parkinson's Disease, which is fully referenced, and nearly 800 pages long, is the most comprehensive book concerning Parkinson's Disease ever written. It includes its history, famous people with Parkinson's Disease, its complete biochemisty, cytology and cytological effects, anatomy and anatomical effects, physiology and physiological effects, symptoms (of every system in the body), diagnosis methods (observational, technological, chemical), biochemical causes, toxic causes, genetic causes, pharmacological causes, medical causes, treatments (biochemical, pharmacological, surgical, natural, exercise methods, technological methods), organisations, web sites. CLICK HERE FOR MORE DETAILS

8th August 2018 - New research

GARCINOL - A FUTURE MAO INHIBITOR FOR PARKINSON'S DISEASE        

MAO inhibitors are often prescribed for Parkinson's Disease. MAO inhibitors help to maintain dopamine levels by inhibiting the enzyme Monoamine Oxidase (MAO). It is primarily low dopamine levels that cause Parkinson's Disease. The main MAO inhibitors in use are selegiline, rasagiline and safinamide. For more information go to : selegiline , rasagiline , safinamide . Researchers have assessed Garcinol, which originates from plant species. For more information go to : garcinol

The present study identified Garcinol as a potential candidate in the treatment of Parkinson's Disease by virtue of its exorbitant MAO-B inhibitory potential. The inhibitory potential is comparable to the known MAO-B inhibitors, which was evaluated using molecular docking technique.

Additionally, Garcinol was found to have potential as a COMT inhibitor, which the existing MAO inhibitors don't have. COMT inhibitors are another type of Parkinson's Disease drug. It was also found to have known antioxidant and anti-inflammatory potential.

Reference : Medical Hypotheses [2018] 117 : 54-58 (M.K.Mazumder, R.Paul, B.C.Phukan, A.Dutta, J.Chakrabarty, P.Bhattacharya, A.Borah)  Complete abstract  In order to refer to this article on its own click here

31st July 2018 - New research

BREATH TEST FOR EARLY PARKINSON'S DISEASE

Researchers have tested a sensor to detect early Parkinson's Disease solely by using the breath of the patients. A device was previously developed that had 40 sensors based on gold nanoparticles. Each sensor had a different chemical attached to it that could bind certain volatile molecules in the breath. The device detected differences in the exhaled breath of people already being treated for Parkinson's Disease. So it was assessed whether the device could detect differences in the breath of people with early or untreated Parkinson's Disease.

The sensitivity, specificity, and accuracy values of the sensor array to detect Parkinson's Disease when compared to people who did not have Parkinson's Disease controls were 79%, (sensitivity), 84% (specificity), and 81% (accuracy).

The results were less than when using the more expensive Midbrain ultrasonography, which gave results of 93% (sensitivity), 90% (specificity), and 92% (accuracy). However, the results were considerably better than when using smell detection tests which gave far lesser results : 62% (sensitivity), 89% (specificity), and 73% (accuracy). So although the device needs to be improved and validated by larger studies, the researchers say that it has potential as a small, portable system to screen at-risk individuals without the need for highly trained specialists.

Reference : : Journal of Neurology [2018] Jun 26 [Epub ahead of print] (A.Romagnolo, M.Fabbri, A.Merola, E.Montanaro, S.Palermo, T.Martone, A.Seresini, S.Goldwurm, M.G. Rizzone, L.Lopiano)   Complete abstract  In order to refer to this article on its own click here

31st July 2018 - News report

ALAN ALDA DIAGNOSED WITH PARKINSON'S DISEASE

Alan Alda, the 82 year old Hollywood actor, has announced that he has had Parkinson's Disease since 2015.  His is a six-time Emmy Award winner, a Golden Globe Award winner, and was nominated for the Academy Award for Best Supporting Actor. He is best known for the long running tv series, the American comedy drama, M*A*S*H, and the films : The Aviator, Crimes and Misdemeanors, Manhattan Murder Mystery, and The Four Seasons. He revealed his diagnosis in 2015 in an interview with CBS This Morning, where he discussed the “full life” he’s lived since then. He decided to reveal his Parkinson's Disease diagnosis after he noticed during a TV appearance that his thumb was twitching.  For more information go to the news report :  News report 

8th July 2018 - New research

AN ASSESSMENT OF HAVING PARKINSON'S DISEASE FOR 35 YEARS

An assessment was carried out of the clinical, neuropsychological, electrophysiological, and neuroimaging features of Parkinson's Disease since the onset of motor symptoms in people who had Parkinson's Disease for over 35 years.

The patients who were assessed had been treated with L-dopa and subthalamic nucleus deep brain stimulation (STN-DBS). Despite the amount of time that had elapsed there was still a sustained motor response to L-dopa (range 14%-35%), a sustained response to STN-DBS (range 23%-38%), and also to L-dopa plus STN-DBS (37%-63%). There were mild to moderate non-motor symptoms (within a range of 19 to 83 on a scale of 0 to 360), and autonomic dysfunction (within a range of 8-28 on a scale of 0-69). Two patients were demented, one had mild cognitive impairment, and two were cognitively preserved. Three of the patients had a peripheral neuropathy and two had a moderate-to-severe autonomic neuropathy. Their genetic tests were unremarkable.

Even after more than 35 years of having Parkinson's Disease, L-dopa and STN-DBS remained effective to some extent, and were even more effective in combination, on the cardinal symptoms of Parkinson's Disease.

Reference : Journal of Neurology [2018] Jun 26 [Epub ahead of print] (A.Romagnolo, M.Fabbri, A.Merola, E.Montanaro, S.Palermo, T.Martone, A.Seresini, S.Goldwurm, M.G. Rizzone, L.Lopiano)   Complete abstract  In order to refer to this article on its own click here

15th June 2018 - New research

LRP10 - A NEW GENETIC FORM OF PARKINSON'S DISEASE

A new genetic form of Parkinson's Disease has been discovered called LRP10. A small proportion of cases of Parkinson's Disease have a genetic cause. Most of them make Parkinson's Disease more likely rather than inevitable. Genetic disorders normally occur due to inheritance, either autosomal recessive (from both parents) or autosomal dominant (from one parent), but can arise spontaneously. Having relatives with Parkinson's Disease does not mean that it has been inherited, because relatives can have similar environmental factors. For more information concerning genetic causes go to :  Genetic causes of Parkinson's Disease

The gene, which is called LRP10, is on Chromosome 14. The type of inheritance is unknown. This genetic form of Parkinson's Disease was found in Italian individuals and somebody from Taiwan but that does not mean that other nationalities are not affected. Of those people that had rare and potentially pathogenic variants, four of them had Parkinson's Disease, two of them had Parkinson's Disease with dementia, and two of them had Parkinson's Disease with dementia and Lewy bodies. The findings implicate LRP10 gene defects in the development of inherited forms of a-synucleinopathies. Being newly discovered there are no genetic tests for LRP10.

Reference : Lancet Neurology [2018] Jun 6 [Epub ahead of print] (M.Quadri, W. Mandemakers, M.M.Grochowska, R.Masius, H.Geut, E.Fabrizio, G.J.Breedveld, D. Kuipers, M.Minneboo, L.J.M.Vergouw, A.Carreras Mascaro, E.Yonova-Doing, E.Simons, T.Zhao)  Complete abstract  In order to refer to this article on its own click here

5th June 2018 - New research

ADAPTIVE DEEP BRAIN STIMULATION FOR PARKINSON'S DISEASE

Deep Brain Stimulation is the most effective form of surgery for Parkinson's Disease. It involves the use of electrodes that are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS uses a surgically implanted, battery-operated medical device, which is similar to a heart pacemaker and approximately the size of a stopwatch. For more information go to :  Deep Brain Stimulation

The existing method of DBS is delivered continuously. Adjustments to the patient's changing symptoms must be made manually by a trained clinician. Consequently, patients may be subjected to energy intensive settings when they are not needed, therby resulting in adverse effects such as dyskinesia. One solution is 'adaptive' DBS, in which stimulation is constantly modified naturally by neural signals that vary according to the severity of muscular symptoms or adverse effects. An assessment that was carried out using brain sensing to control the brain stimulation was demonstrated in two patients with Parkinson's Disease.

In in-clinic testing, energy savings were substantial (38%-45%), and therapeutic efficacy was maintained. This is the first demonstration of adaptive DBS in Parkinson's Disease using a fully implanted device and neural sensing.

Reference : Journal of Neural Engineering [2018] 15 (4) : 046006 (N.C.Swann, C.de Hemptinne, M.C.Thompson, S.Miocinovic, A.M.Miller, R.Gilron, J.L.Ostrem, H.J.Chizeck, P.A.Starr) Complete abstract  In order to refer to this article on its own click here

29th May 2018 - New clinical trial

MICHAEL J.FOX FOUNDATION FUNDS ALK4290 FOR PARKINSON'S DISEASE

Alkahest, a clinical-stage biotechnology company, has been awarded a grant from The Michael J.Fox Foundation for the “Development of ALK4290 as a novel PD therapeutic”.  

This project will focus on the mechanisms underlying immune cell involvement in Parkinson’s Disease, assessing the link between neuroinflammation and disease progression. ALK4290 is a novel, orally-available, small molecule that has been well-tolerated in previous clinical studies. They will evaluate the effect of ALK4290 in two pre-clinical models relevant to Parkinson's Disease biology. A toxin-induced and a transgenic model of disease will allow them to assess the efficacy of the compound on Parkinson's Disease-relevant processes.  For more information go to  Alkahest  

24th May 2018 - New cliniacl trial

DEMENTIA DRUG FOR REDUCING FALLS IN PARKINSON'S DISEASE

A UK-wide trial into Parkinson’s Disease led by Royal United Hospitals Bath NHS Foundation Trust and the University of Bristol will assess whether a commonly prescribed dementia drug (a cholinesterase inhibitor) could prevent debilitating falls for people with Parkinson's Disease. Falls are a frequent complication in people with Parkinson’s Disease. Earlier phase trials which showed that cholinesterase inhibitors have the potential to almost halve the number of falls in people with Parkinson's Disease and improve the regularity of their walking, speed, and balance. For more information go to  University of Bristol  

11th May 2018 - New research

METOCLOPRAMIDE INCREASES THE RISK OF PARKINSON'S DISEASE

Metoclopramide is Dopamine D2 receptor antagonist. Dopamine antagonists inhibit the dopamine receptors. Metoclopramide is a drug used mostly for stomach and esophageal problems. It increases muscle contractions in the upper digestive tract. This speeds up the rate at which the stomach empties into the intestines. For more information go to  Metoclopramide  The risk of Parkinson's Disease is increased 1.73 times in standard exposure users of metoclopramide, and 3.15 times in high exposure users. The average increase in risk of Parkinson's Disease was 2.16 times normal.  That means that the increased risk is still low.

However, since long-duration exposure accounts for the majority of users and parkinsonism in the high-exposure group, physicians are advised to avoid prescribing metoclopramide for morer than 5 days, even if the daily dose is 30 mg.

Reference : British Journal of Clinical Pharmacology [2018] May 10 [Epub ahead of print] (S.C.Tsai, S.Y.Sheu, L.N.Chien, H.C.Lee, E.J.Yuan, R.Y.Yuan) Complete abstract 

25th April 2018 - New research

MICROTABLET DISPENSER FOR MORE PRECISE L-DOPA DOSAGE

A study has assessed the effect of introducing a microtablet dose dispenser and adjusting doses based on the monitoring of motor symptoms in people with Parkinson's Disease. Forms of L-dopa are usually limited to certain doses and are consequently not adaptable to needs. A microtablet dose dispenser enables more precise doses of L-dopa.

Daytime doses of L-dopa were replaced with L-dopa / carbidopa microtablets, 5mg / 1.25 mg delivered from a dose dispenser device with programmable reminders. After two weeks, doses were adjusted based on ambulatory accelerometry and clinical monitoring. The daily L-dopa dose was increased by 15% from period 1 to 2, and the dose interval was reduced by 12%. The MDS-UPDRS parts II and III, disease-specific quality of life (PDQ-8), wearing-off symptoms (WOQ-19), and nonmotor symptoms improved after dose increases.

Evaluation of accelerometry results demonstrated improvement in 60% of subjects and worsening in 25% of them. The introduction of an L-dopa microtablet dispenser and accelerometry aided dose adjustments Parkinson's Disease improve symptoms and quality of life in the short term.

Reference : CNS Neuroscience and Therapeutics [2018] 24 (5) : 439-447 (D.Jan Johansson, A.Ericsson, A.Johansson, A.Medvedev, D.Nyholm, F.Ohlsson, M.Senek, J.Spira, I.Thomas, J.Westin, F.Bergquist) Complete abstract  In order to refer to this article on its own click here

20th April 2018 - New research

MILD BRAIN INJURY INCREASES RISK OF PARKINSON'S DISEASE

An assessment was made of the risk of developing Parkinson Disease after traumatic brain injury (TBI), including mild TBI. This was assessed among care recipients in the Veterans Health Administration with over 300,000 patients. Compared to those people with no traumatic brain injury, those people with traumatic brain injury (TBI) had a higher incidence of Parkinson's Disease : no TBI (0.31%), mild TBI (0.47%), all severities of TBI (0.58%), moderate to severe TBI (0.75%). The increased likelihood of TBI was 1.56 times in mild TBI, 1.71 times in all severities of TBI) and 1.83 times in moderate to severe TBI. So even mild traumatic brain injury is associated with a 56% increased risk of developing Parkinson's Disease.

Reference : Neurology [2018] Apr 18 [Epub ahead of print] (R.C.Gardner, A.L.Byers, D.E.Barnes, Y.Li, J.Boscardin, K.Yaffe)  Complete abstract 

20th March 2018 - New research

EXTENDED RELEASE AMANTADINE FOR DYSKINESIA IN PARKINSON'S DISEASE

Chronic use of L-dopa is associated with dyskinesia. ADS-5102 (amantadine) extended-release (ER) capsules (GOCOVRITM) is a recent approved treatment for dyskinesia in Parkinson's Disease. ADS-5102 is a high-dose, ER formulation of amantadine, administered orally once daily at bedtime, that achieves high plasma drug concentrations throughout the day. After 12 weeks, the score on the Unified Dyskinesia Rating Scale was reduced by 17.7 in comparison to 7.6 on a placebo. The mean change in OFF time was a reduction of 35 minutes per day. The most common adverse events were hallucinations, dizziness, dry mouth, peripheral edema, constipation, falls, and orthostatic hypotension.

Reference : CNS Drugs [2018] Mar 12 [Epub ahead of print] (L.W.Elmer, J.L.Juncos, C.Singer, D.D.Truong, S.R.Criswell, S.Parashos, L.Felt, R.Johnson, R.Patni) Complete abstract 

24th February 2018 - New research

THE RETINA DETERIORATES IN PARKINSON'S DISEASE

Studies using OCT (optical coherence tomography) have reported alterations in the retinal nerve fiber layer (RNFL) in people with Parkinson's Disease. The average retinal nerve fiber layer (RNFL) thickness, total macular thickness, and macular volume have been found to be decreased in people with Parkinson's Disease, subsequently decreased even further, and tended to get worse with age. The macula is an area near the centre of the retina in the eye. The progression of Parkinson's Disease is associated with pronounced retinal structure changes, which can be quantified by OCT (optical coherence tomography).

A single group of dopaminergic neurons (A17) has been found in the retina, which is why it is affected in Parkinson's Disease. Patterns of RNFL (retinal nerve fibre layer) and macular damage detected by OCT could consequently be a useful biomarker for evaluating the progression of PD.

Reference : Journal of Parkinsons Disease [2018] 8 (1) : 85-92 (L.J.Ma, L.L.Xu, C.J.Mao, Y.T.Fu, X.Y.Ji, Y.Shen, J.Chen, Y.P.Yang, C.F.Liu) Complete abstract 

28th January 2018 - New research

LONG TERM EFFECTS OF RASAGILINE ON PARKINSON'S DISEASE

Rasagiline is a MAO inhibitor, sold as Azilect, which is used for the treatment of Parkinson's Disease. For more information go to Azilect In the long term there has been found to be no advantage in starting the use of rasagiline early rather than delaying its use. After three years the Parkinson's Disease symptoms scores did not differ between those who started early and those who delayed its use. In both groups there was a worsening of their symptoms. Additionally, 43% of patients had onset of unsteady gait and balance impairment, 35% had fallen, 26% had freezing of gait, and 33% had cognitive decline.

Reference : Movement Disorders [2016] 31 (10) : 1489-1496 -274 (O.Rascol, R.A.Hauser, F.Stocchi, C.J.Fitzer-Attas, Y.Sidi, V.Abler, C.W.Olanow) Complete abstract  In order to refer to this article on its own click here

25th January 2018 - New research

HIGH LEVELS OF VITAMIN B6 INTERFERE WITH L-DOPA IN PARKINSON'S DISEASE

Vitamin B6 (pyridoxine) is essential for health. It is especially important for Parkinson's Disease because the brain's own formation of L-dopa is dependent on sufficient levels of vitamin B6. However, high levels of vitamin B6 can lessen the effect of L-dopa and thereby make Parkinson's Disease symptoms worse. A systematic review of unacceptable levels of vitamin B6 among L-dopa users was carried out. The results indicated that a vitamin B6 intake of more than 50 mg per day could reduce the efficacy of L-dopa. Such levels are not necessary for optimal health because the daily requirement of vitamin B6 is up to 2mg per day. So it is important that people taking L-dopa for Parkinson's Disease should ensure that any supplements they are taking should not exceed 50mg vitamin B6 (pyridoxine) per day.

Reference : Shokuhin Eiseigaku Zasshi [2017] 58 (6) : 268-274 (Y.Sato, C.Yasumiishi, T.Chiba, K.Umegaki) Complete abstract  In order to refer to this article on its own click here

23rd January 2018 - New research

ALPHA-SYNUCLEIN DOES NOT INDICATE PARKINSON'S DISEASE

Although it is sometimes claimed that an accumulation of alpha-synuclein causes Parkinson's Disease, Parkinson's Disease instead can cause alpha-synuclein to accumulate. It has been suggested that alpha-synuclein could therefore be a valuable biomarker for Parkinson's Disease. So the levels of alpha-synuclein in the plasma was assessed in various types of Parkinson's Disease. Alpha-synuclein is commonly found in the brain. For more information go to : Alpha-synuclein

Methods: People with Parkinson's Disease were compared to healthy volunteers who were matched by age and gender. They were assessed with the use of Parkinson's Disease symptom scales.

Results : Levels of alpha-synuclein did not differ significantly between people with Parkinson's Disease and people who did not have Parkinson's Disease. There was no difference between different subtypes. Yet there was an inverse correlation between alpha-synuclein and the Postural Instability and Gait Disorder (PIGD) subtype.

Conclusions : Plasma alpha-synuclein levels are not valuable biomarkers of Parkinson's Disease. It does not differ in the subtypes of Parkinson's Disease either. However, there is an inverse relation between plasma alpha-synuclein levels level and the severity of Parkinson's Disease in the Postural Instability and Gait Disorder (PIGD) subtype.

Reference : Neurologia i Neurochirurgia Polska [2017] Nov 21 [Epub ahead of print] (M. Malec-Litwinowicz, A.Plewka, D.Plewka, E.Bogunia, M.Morek, A.Szczudlik, M. Szubiga, M.Rudzinska-Bar) Complete abstract  In order to refer to this article on its own click here

12th January 2018 - New research

SEXUAL DYSFUNCTION IN WOMEN WITH PARKINSON'S DISEASE

In women with Parkinson's Disease there can be a profound impairment in sexual arousal, behaviour, orgasm, sexual satisfaction and sex drive. The objectives of this study were to assess the level of sexual function in women with Parkinson's Disease, and the description of sexual dysfunctions.

Women with Parkinson's Disease were assessed over a broad age range of 40 to 89 years. According to the Female Sexual Function Index, sexual dysfunction was present in 87% of women with Parkinson's Disease, but this was not a lot more than the dysfunction that occurred in 79% of women who did not have Parkinson's Disease. However, according to the Sexual Dysfunction Inventory the difference was greater, with 57% of women with Parkinson's Disease having sexual dysfunction, and in only 22% of women without Parkinson's Disease.

Sexual dysfunction was found to be more prevalent in women with Parkinson's Disease and is predicted by older age and the severity of depressive symptoms.

Reference : Movement Disorders [2016] 31 (11) : 1685-1693 (S.Varanda, J.Ribeiro da Silva, A.S.Costa, C.Amorim de Carvalho, J.N.Alves, M.Rodrigues, G.Carneiro) Complete abstract  In order to refer to this article on its own click here

6th January 2018 - New research

L-DOPA INHALER RAPIDLY IMPROVES PARKINSON'S DISEASE

Background : The L-dopa inhaler CVT-301 is presently being assessed for its use in Parkinson's Disease. It is designed to deliver a precise dose of a dry powder formulation of L-dopa. Inhaled L-dopa enters the body through the lungs and then reaches the brain far more quickly by bypassing the digestive system. For more information go to : CVT-301

Methods : Patients used the L-dopa inhaler CVT-301 up to 3 times per day for OFF episodes. After 2 weeks, the study-drug dose was increased from 35mg to 50 mg. The patients were assessed after 10, 20, 30, and 60 minutes. Results: The L-dopa inhaler was used at an average of 2.1 times per day. The UPDRS Part III score (Parkinson's Disease symptoms) clearly improved. A treatment effect was already evident after only 10 minutes.  The most frequently reported adverse events in those using CVT-301 were dizziness, cough, and nausea, each in 7% of patients.

Conclusion :  As the effect was already seen after 10 minutes, which is the shortest time assessed, the effect could be even quicker. Consequently, CVT-301 could become of widespread use in Parkinson's Disease for when a quick effect is needed.

Reference : Movement Disorders [2016] 31 (9) : 1356-1365 (P.A.LeWitt, R.A.Hauser, D.G. Grosset, F.Stocchi, M.H.Saint-Hilaire, A.Ellenbogen, M.Leinonen, N.B.Hampson, T.DeFeo-Fraulini, M.I.Freed, K.D.Kieburtz) Complete abstract  In order to refer to this article on its own click here

5th January 2018 - New research

CAFFEINE LEVELS CAN INDICATE EARLY PARKINSON'S DISEASE

Caffeine was assessed as a possible means of diagnosing Parkinson's Disease. Caffeine is found in coffee, and to a lesser extent in tea, yerba mate, cola drinks, cocoa, and chocolate. The levels of caffeine and 9 of its 11 metabolites were found to be significantly decreased in people with early Parkinson's Disease. This was unrelated to each person's caffeine intake and the severity of their Parkinson's Disease. Caffeine levels were also reduced in people with Parkinson's Disease who had motor problems. It has been suggested that caffeine and its metabolites are therefore promising indicators of early Parkinson's Disease.

Reference : Neurology [2018] Jan 3 [Epub ahead of print] (M.Fujimaki, S.Saiki, Y.Li, N.Kaga, H.Taka, T.Hatano, K.I.Ishikawa, Y.Oji, A.Mori, A.Okuzumi, T.Koinuma, S.I.Ueno, Y.Imamachi, T.Ueno, Y.Miura, M.Funayama, N.Hattori) Complete abstract 

31st December 2017 - New research

CAMICINAL INCREASES L-DOPA LEVELS IN PARKINSON'S DISEASE

Delayed gastric emptying can impair absorption of L-dopa, thereby contributing to motor fluctuations. Camicinal (GSK962040), is a gastroprokinetic, which is being assessed for its effect on the absorption of L-dopa and the symptoms of Parkinson's Disease. Gastroprokinetic drugs increase the movement of ingested material through the GI tract.

Patients were given either 50mg camicinal daily for 7 to 9 days or were taking a placebo. Average time to reach maximum L-dopa concentration by taking camicinal was reduced, indicating more rapid absorption of L-dopa.

Camicinal resulted in significant reduction in OFF time, reducing it by 2 hours 18 minutes. There was a significant increase in ON time, increasing it by 1 hour 52 minutes. There was also a significant decrease in mean total MDS-UPDRS score (Parkinson's Disease symptoms). Camicinal treatment was generally well tolerated.

Parkinson's Disease symptom improvement with the use of camicinal occurred in parallel with a more rapid absorption of L-dopa. This study provides evidence of an improvement of the motor response to L-dopa in people with Parkinson's Disease treated with camicinal

Reference : Movement Disorders [2017] Dec 26 [Epub ahead of print] (S.L.Marrinan, T.Otiker, L.S.Vasist, R.A.Gibson, B.K.Sarai, M.E.Barton, D.B.Richards, P.M.Hellström, D.Nyholm, G.E.Dukes, D.J.Burn) Complete abstract  In order to refer to this article on its own click here

27th December 2017 - New research

ORALLY DISSOLVING FILM FOR TAKING ROPINIROLE

Ropinirole is a dopamine agonist used for Parkinson's Disease. It is sold as Requip, Repreve, Ronirol, and Adartrel. For more information go to For more information go to : Requip

However, ropinirole undergoes extensive metabolism, resulting in a low oral bioavailability. The necessity of frequent administration due to the short half-life of ropinirole may also lessen patient compliance. There is consequently a pressing need to devise formulations for the delivery of ropinirole that allow simple and easy administration.

It was aimed at overcoming all these challenges by using orally-dissolving films via sublingual delivery (under the tongue) or buccal delivery (via tissues that line the mouth).  The ropinirole oral film was found to be non-toxic, exhibited fast disintegration and dissolution, and was also physically stable. Upon buccal and sublingual administration of the oral films, ropinirole reached the systemic circulation within 15 minutes and bioavailability was significantly improved. This may be attributable to the avoidance of first-pass metabolism via absorption through the oral cavity.

In conclusion, the ropinirole oral film improved bioavailability after sublingual or buccal administration. This formulation potentially overcomes biopharmaceutical challenges and provides a convenient means of administration of ropinirole and also other Parkinson's Disease drugs.

Reference : Colloids and Surfaces, B Biointerfaces [2017] 163 : 9-18 [Epub ahead of print] (K.L.Lai, Y.Fang, H.Han, Q.Li, S.Zhang, H.Y.Li, S.F.Chow, T.N.Lam, W.Y.T.Lee) Complete abstract  In order to refer to this article on its own click here

22nd December 2017 - New research

LASER SHOES FOR PARKINSON'S DISEASE

Laser shoes have been developed to help with the freezing that can occur in Parkinson's Disease. When freezing (freezing of gait) occurs, the person finds themself unable to take a step despite willing themselves to walk forward. This can occur for anything from a few seconds to over a minute and can cause a person to lose their balance and fall over. Each laser shoe has a projection device mounted to the toe that produces a line about 18 inches (half a metre) ahead, towards which the user can then step. Patients with Parkinson's Disease who had freezing of gait were assessed in "off" and also "on" medication states.

Cueing using laser shoes was associated with a significant reduction in freezing of gait episodes both during "off" medication (45%) and "on" (37%) medication. Moreover, laser shoes significantly reduce the time frozen by 56% during "off" medication, and 51% during "on" medication. These effects were paralleled by the patients' positive subjective experience on the efficacy of laser shoes.

These findings demonstrate the efficacy of laser shoes and so offer a promising potential to deliver cueing for people with freezing of gait.

Reference : Neurology [2017] Dec 20 [Epub ahead of print] (C.Barthel, J.Nonnekes, M.van Helvert, R.Haan, A.Janssen, A.Delval, V.Weerdesteyn, B.Debû, R.van Wezel, B.R.Bloem, M.U.Ferraye) Complete abstract  In order to refer to this article on its own click here

12th December 2017 - New research

EARLY WEIGHT LOSS IN PARKINSON'S DISEASE

Weight changes over time in people with Parkinson's Disease and in those with atypical parkinsonism and can be associated with an increased risk of dependency, dementia and death.

People with Parkinson's Disease are generally lighter than average. People with atypical Parkinsonism normally had lower body weights than people with Parkinson's Disease. Weight loss was greater in people with Parkinson's Disease and even greater in people with atypical Parkinsonism. Only age was independently associated with significant weight loss, making it almost twice as likely as people age. When people with Parkinson's Disease lost weight within a year of diagnosis it was associated with a more than doubling of an increased risk of dependency, and a more than tripling of the risk of dementia, and a more doubling of the risk of death.

Reference : Neurology [2017] 89 (22) : 2254-2261 (K.Cumming, A.D.Macleod, P.K.Myint, C.E.Counsell) Complete abstract  In order to refer to this article on its own click here

30th November 2017 - New research

EFFICACY AND SAFETY OF PERAMPANEL IN PARKINSON'S DISEASE

Perampanel is a non-competitive AMPA-type glutamate receptor antagonist, being assessed for use in the treatement of Parkinson's Disease. An extensive assessment of perampanel, including trials involving thousands of patients was carried out concerning its efficacy and safety. Four daily doses were assessed : 0.5mg, 1mg, 2mg, 4mg. However, no difference was found between the effect of perampanel and the effect of a placebo. Therefore, perampanel was found to be ineffective. The adverse effects were also similar for perampanel and a placebo, at least confriming its safety.

Reference : British Journal of Pharmacology [2017] Jul 1 [Epub ahead of print] (D.Lindenbach, B.Das, M.Conti, S.M.Meadows, A.K.Dutta, C.Bishop)  Complete abstract 

27th November 2017 - New research

BLADDER AND BOWEL SYMPTOMS IN PARKINSON'S DISEASE

An assessment was made of the prevalence of urinary and bowel symptoms, such as urinary incontinence and constipation in people with early Parkinson's Disease. Prevalent bladder symptoms (urinary incontinence and nighttime voiding) and bowel symptoms (constipation and fecal incontinence) were defined as occurring at least sometimes.

Constipation occurred three times more often in people with early Parkinson's Disease (in around 32% of people). Urinary incontinence occurred three times more often in people with early Parkinson's Disease (in around 26% of people). Prevalent nighttime urination was also high (in around 82% of people), but was little different in older people who did not have Parkinson's Disease. The likelihood of urinary incontinence and constipation were significantly higher in early Parkinson's Disease even after adjusting for age, sex, cognition, depression, and anxiety medication usage. While constipation is known to precede the diagnosis of Parkinson's Disease, the results suggest that the occurrence of urinary incontinence is also elevated in early Parkinson's Disease.

Reference : Neurourology and Urodynamics 2017 Nov 2 [Epub ahead of print] (M.C.Serra, A.Landry, J.L.Juncos, A.D.Markland, K.L.Burgio, P.S.Goode, T.M.Johnson, C.P.Vaughan) Complete abstract  In order to refer to this article on its own click here

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 civil rights demonstrations with Martin Luther King. 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 [2017] 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 [2017] 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 25% greater with drivers who had Parkinson's Disease and so would not suggest a need for most people with Parkinson's Disease to initially cease driving due to errors they made. When the tests were repeated those people with Parkinson's Disease performed similarly to those people without 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.

Reference : Neurology [2017] Oct 11 [Epub ahead of print] (E.Y.Uc, M.Rizzo, A.M.J. O'Shea, S.W.Anderson, J.D.Dawson) Complete abstract   In order to refer to this article on its own click here

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.

Plasma 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). Plasma alpha-synuclein levels were significantly higher in people with Parkinson's Disease who had dementia than in people with Parkinson's Disease who 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 [2017] 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. Parkinson's Disease that can cause an accumulation of α-synuclein. The effect of Salbutamol on Parkinson's Disease may be due to β2-adrenoreceptor (β2AR) agonists also having an anti-cholinergic effect. Anti-cholinergics are used for Parkinson's Disease.

Reference : Science [2017] 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. It appears 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 [2017] 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.

Reference : Environment International [2017] Aug 2 [Epub ahead of print] (S.Narayan, Z.Liew, J.M.Bronstein, B.Ritz)  Complete abstract   In order to refer to this article on its own click here

8th August 2017 - New book

THE ENLIGHTENED MR. PARKINSON : THE PIONEERING LIFE OF A FORGOTTEN SURGEON

Cherry Lewis

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 place in history with a portrait of him 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 exenatide and worsened in people taking a placebo.  Although it is claimed exenatide can slow deterioration 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.

Reference : The Lancet [2017] 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) Complete abstract  In order to refer to this article on its own click here
              

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 [2017] 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 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 active 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 disability levels, especifically mood, memory, and fatigue.

Reference : Complementary Therapies in Medicine [2017] 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. 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 clinical trial of 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 restorative 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. 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

People with Parkinson's Disease had DBS initiated at either 1 or 3 months after surgery. Safety and efficacy of the treatment were compared between on and off medication states 3 months after surgery. Outcome measures included analysis of Unified Parkinson's Disease Rating Scale (UPDRS) scores, duration of "on" periods, and equivalent doses of L-dopa. Three months after surgery, there had been a very significant decrease in the UPDRS (Parkinson's Disease) motor scores. Bilateral wireless programming STN-DBS was found to be safe and effective for people with Parkinson's Disease when medical management had failed to restore motor function.

Reference : Stereotactic and Functional Neurosurgery [2017] 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.

No statistically significant association was observed overall for particulate matter (PM) or nitrogen dioxide (NO2) exposures and the risk of Parkinson's Disease. However, a relationship was observed when the size of the particles was considered. A higher risk of Parkinson's Disease (1.65 times greater) was associated with higher exposure to larger particles (PM10). A higher risk of Park(1.29 times) was also associated with exposure to smaller particles (PM2.5). Women were more affected than men. Consequently, pollution, especially larger particles, is the cause of a moderate increase in the risk of Parkinson's Disease. The could be higher when the exposures to pollution are more intense or more prolonged.

Reference : Environmental Health Perspectives [2016] 124 (11) : 1759-1765 (R.Liu, M.T. Young, J.C.Chen, J.D.Kaufman, H.Chen)  Complete abstract    In order to refer to this article on its own click here

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

The use of L-dopa is limited by wearing off and dyskinesias. The objective of this study was to investigate the efficacy and safety of safinamide in L-dopa treated patients who had motor fluctuations. If no tolerability issues arose by day 14, the starting dose, 50 mg, was increased to 100 mg. When taking safinamide, the mean change in daily on time without dyskinesia 2.80 hours. However, this was not much different from the effect that a placebo had. The most frequently reported adverse event was dyskinesia (14%], and as a severe event (2%). These results are consistent with previous studies in which the increase in "on" time beyond that of a placebo was only 40 minutes for 50mg safinamide, and 50 minutes for 100mg safinamide. In order to refer to this article on its own click here

Reference : JAMA Neurology [2017] 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.

People with Parkinson's Disease were assessed who had undergone LCAS treatment to alleviate motor complications that were not controlled by optimised conventional Parkinson's Disease treatments. The three main reasons for discontinuation of LCAS treatment were worsening of wearing-off symptoms, persistent dyskinesia, and poor drug adherence. However, there were a small number of each of these. Around 37% of people maintained the LCAS treatment after 12 months. In those people, on time without dyskinesia significantly increased from 33% to 57% after the initiation of LCAS treatment. Around 31% of patients were still receiving LCAS treatment after 30 months. In order to refer to this article on its own click here

Reference : Journal of Neurological Science [2017] 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).

The Most people with Parkinson's Disease (62%) experienced dysphagia (difficult swallowing), which probably contributed to weight loss in 41% of people because they were unable to eat as much. The prevalence of other symptoms was heartburn (37%), regurgitation (31%), chest pain (28%), and odynophagia (painful swallowing) (6%). Problems in the esophagus were also common. The esophagus is through which food passes from the mouth to the stomach. The most common problems were : failure by the esophagus to contract properly (ineffective esophageal peristalsis) (55%), fragmented contraction in the esophagus (fragmented peristalsis) (48%), spasms in the esophagus (DES - diffuse esophageal spasm) (48%), and obstruction of the exit of the esophagus to the stomach (EGJ outflow obstruction) (39%). Each of these causes digestive problems. In order to refer to this article on its own click here

Reference : Diseases of the Esophagus [2017] 30 (4) : 1-6 (A.Su, R.Gandhy, C.Barlow, G.Triadafilopoulos) Nature Biotechnology [2017] 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 [2017] 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 accurately diagnosed, and effectively treated, 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 [2017] 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 [2017] 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.

Reference : Indian Journal of Medical Research [2016] 144 (5) : 682-688 (S.Pandey, H.Kumar) Complete abstract  In order to refer to this article on its own click here