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MARCH 2012

                                                                                                                                                 

25th March 2012 - New research

THE WORLD'S HIGHEST PREVALENCE OF PARKINSON'S DISEASE

Neuroepidemiology [2012] 38 (3) : 138-147 (Kruja J, Beghi E, Zerbi D, Dobi D, Kuqo A, Zekja I, Mijo S, Kapisyzi M, Messina P.) Complete abstract

Albania has been found to be the country with the world's highest prevalence of Parkinson's Disease by far. The prevalence figures for Parkinsonism were found to be 800 per 100,000. To put that in perspective, the countries with the next highest prevalence of Parkinson's Disease (per 100,000) are the U.S.A. with 329 and Israel with 256. Parkinsonism includes some other disorders. So the Albanian figure for only Parkinson's Disease would be lower, but still far higher than any other country. The prevalence of neurological disorders in Albania was found to be high generally. It was not only Parkinson's Disease that is common there. Albania is one of the poorest nations in Europe but poverty is not related to the prevalence of Parkinson's Disease. There are isolated communities elsewhere that have a very high prevalence of Parkinson's Disease. This includes the Amish religious community in the U.S.A., the Parsi community of Mumbai, and the vicinities of ferromanganese plants near Brescia in Italy.  For more information go to the Prevalence of Parkinson's Disease. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

22nd March 2012 - News release

CLINICAL TRIAL RESULTS - DIPRAGLURANT FOR PARKINSON'S DISEASE DYSKINESIA

Addex Therapeutics have announced data from a Phase II clinical trial of Dipraglurant in people with Parkinson's Disease who have dyskinesia caused by L-dopa. Dipraglurant is an orally taken drug presently being developed that inhibits glutamate receptor 5. For more information go to Dipraglurant. L-dopa induced dyskinesias are very commonly observed during the long-term treatment of people with Parkinson's Disease. No drug is presently approved for its treatment. The Michael J. Fox Foundation, who have supported the clinical trial, consequently suggest that it satisfies an important medical need.

Dipraglurant met its primary objective of demonstrating safety and tolerability in people with Parkinson's Disease. The incidence of adverse events was slightly higher in those taking Dipraglurant (88%) than in those taking a placebo (75%). Adverse events typical with drugs of this kind, such as vertigo, visual disturbances, and feeling drunk, were seen in less than 10% of people taking Dipraglurant, but were not severe. Exploratory efficacy data showed an anti-dyskinetic effect. People taking Dipraglurant had as much as 70 minutes more on-time without dyskinesia than people taking a placebo. During Week 4, patients also reported a reduction in daily off-time of 50 minutes, suggesting an effect on parkinsonian motor symptoms in addition to the observed reductions in dyskinesia. For more information go to Addex Therapeutics. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

14th March 2012 - New research

L-DOPA PRODRUG CLINICAL TRIAL RESULTS

Clinical Neuropharmacology [2012] Mar 7 [Epub ahead of print] (Lewitt PA, Ellenbogen A, Chen D, Lal R, McGuire K, Zomorodi K, Luo W, Huff FJ.) Complete abstract

XP21279 is a new chemical entity being developed for the treatment of Parkinson's Disease. XP21279 uses naturally-occurring, high-capacity nutrient transporters in the gastrointestinal tract to generate active, efficient absorption into the body. Once absorbed, XP21279 is rapidly converted into L-Dopa, a drug that acts to replace dopamine. For more information go to Xenoport. The L-dopa prodrug XP21279 aims to replace the use of L-dopa, which has many undesirable effects including its rapid breakdown by gastric and peripheral enzymes, only a short duration in the blood after oral consumption, which leads to fluctuation of drug plasma concentrations when taken frequently, and a limited period for possible absorption from the gastrointestinal tract.

In the clinical trial of XP21279, people with Parkinson's Disease were given either XP21279 with carbidopa (which helps to prevent the breakdown of L-dopa), or L-dopa with carbidopa (which is the same combination in Sinemet). With the use of XP21279 there was significantly less variability in the concentration of L-dopa. XP21279 may therefore provide better control of motor fluctuations. Overall, there was a reduction in daily OFF time. There was also more ON time without troublesome dyskinesia. The average time to ON time was not delayed when using XP21279. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

11th March 2012 - News report

NOBEL PRIZE WINNER DIES WITH PARKINSON'S DISEASE

Nobel Prize winning chemist Frank Sherwood Rowland (1927-2012) died, aged 84, on 10th March 2012 due to the complications of Parkinson's Disease. For more information go to the News report. His research mainly concerned atmospheric chemistry and chemical kinetics. His best known work was the discovery in 1974 that chlorofluorocarbons (CFC's) contribute to the depletion of the ozone layer. In 1978, his discovery led to CFC-based aerosols being banned in the U.S.A.. His discovery then also led to the 1987 Montreal Protocol, an international environmental treaty to stop the production of the CFC-based aerosols. In 1995 he won the Nobel Prize for Chemistry along with Mario Molina and Paul Crutzen for their contribution towards various fields. For more information go to Frank Sherwood Rowland.

 

7th March 2012 - New research

THE DEVELOPMENT OF HALLUCINATIONS IN PARKINSON'S DISEASE

Movement Disorders [2011] 26 (12) : 2196-2000 (Goetz CG, Stebbins GT, Ouyang B.) Complete abstract

Although visual hallucinations on their own are considered classic Parkinson's Disease symptoms, non-visual hallucinations also develop over time, and the combination of visual with non-visual hallucinations dominates in late Parkinson's Disease. The objective of this study was to assess the development and evolution of visual and non-visual hallucinations in people with Parkinson's Disease over 10 years. Over 10 years, visual hallucinations were still found to be more frequent than other forms of hallucinations.

Isolated visual hallucinations dominate the early years of Parkinson's Disease, but visual plus non-visual hallucinations accounted for progressively higher proportions of people with Parkinson's Disease. Hallucination severity was highly associated with somebody currently having visual plus non-visual hallucinations.  After 6 months with Parkinson's Disease, virtually nobody had hallucinations. However, after 4 years, over a quarter (26%) of people with Parkinson's Disease had hallucinations. After 6 years, nearly half (47%) of people with Parkinson's Disease had hallucinations. After 10 years with Parkinson's Disease, 60% of people had hallucinations. Once somebody had both visual and non-visual hallucinations, the risk of continuing to have them was high.

Although hallucinations commonly occur in Parkinson's Disease, hallucinations are not Parkinson's Disease symptoms. They eventually occur because of the effect of dopaminergic drugs such as L-dopa. Because the effects of these drugs on Parkinson's Disease symptoms wears off over time, higher dosages are usually required to have the same effect. These progressively increasing dosages makes hallucinations progressively more likely. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

4th March 2012 - New research

THE EFFECT OF GENDER ON DYSKINESIA

Journal of Neurology [2011] 258 (11) : 2048-2053 (Hassin-Baer S, Molchadski I, Cohen OS, Nitzan Z, Efrati L, Tunkel O, Kozlova E, Korczyn AD.) Complete abstract

L-dopa induced dyskinesias are commonly observed during the long-term treatment of people with Parkinson's Disease. Dyskinesia is involuntary jerking movements as can be seen in this Michael J.Fox video.  The effect of factors other than drugs on the time taken to develop dyskinesias was not known. So researchers assessed factors associated with the time taken for L-dopa induced dyskinesias to appear.

People with L-dopa induced dyskinesias (LID) were younger when Parkinson's Disease first developed. So developing Parkinson's Disease early makes L-dopa induced dyskinesias more likely. A longer time from diagnosis to being treated for Parkinson's Disease also increased the likelihood of developing L-dopa induced dyskinesias. Age and how long somebody had Parkinson's Disease had no effect on the likelihood of developing L-dopa induced dyskinesias. Females were more prone to developing L-dopa induced dyskinesias more quickly, with an average of 4 years rather than 6 years for men. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

3rd March 2012 - New research

CLR01 CLAIMED TO SLOW PARKINSON'S DISEASE

Neurotherapeutics  [2012] Feb 29 [Epub ahead of print] (Prabhudesai S, Sinha S, Attar A, Kotagiri A, Fitzmaurice AG, Lakshmanan R, Ivanova MI, Loo JA, Klärner FG, Schrader T, Stahl M, Bitan G, Bronstein JM.) Complete abstract

Aggregation of α-synuclein in the cells involved in Parkinson's Disease is claimed as being causative in Parkinson's Disease, multiple system atrophy, and dementia with Lewy bodies. A novel "molecular tweezer" termed CLR01 has been described as a potent inhibitor of α-synuclein by preventing it from being formed. In cell cultures CLR01 was shown to greatly lessen α-synuclein. 

To determine whether CLR01 was also protective in animals, the researchers used a zebrafish, which is a type of fish commonly used in Parkinson's Disease research because it is easily manipulated genetically, and because some of its biochemistry is similar to that in humans.  CLR01 significantly improved zebrafish survival, suppressed the aggregation of α-synuclein, and also reduced cell death caused by α-synuclein. This occurred without evidence of toxicity. The authors consequently claimed that CLR01 stopped the progression of Parkinson's Disease in an animal model, and is therefore a promising therapeutic agent for the treatment of Parkinson's Disease.

However, zebrafish do not have Parkinson's Disease. Parkinson's Disease was not simulated in the zebrafish either. There were therefore no measures of whether or not Parkinson's Disease symptoms altered as a result of CLR01. So it could not reasonably be claimed that CLR01 was shown to stop or slow the progression of Parkinson's Disease, even in animals. A lot of the toxicity that could occur in humans would not be detectable in zebrafish either. Researchers measured the effects in terms of α-synuclein, which does not indicate Parkinson's Disease. It occurs in other medical disorders and often fails to occur in Parkinson's Disease. For a printable version of this article click here.  In order to refer to this article on its own click here. 

 

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