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JANUARY 2009

                                                                                                                                                      31st January 2009 - New clinical trial

NEW GLUTAMATE ANTAGONIST CLINICAL TRIAL RESULTS

Addex Pharmaceuticals have announced what they describe as "the successful completion" of Phase I studies of a newly developed modified release formulation of ADX48621. ADX48621 is a glutamate antagonist aimed at treating the dsykinesia caused in Parkinson's Disease by taking L-dopa. The study showed that the new formulation achieved satisfactory pharmacokinetics, safety and tolerability with single and repeat dose administration across the dose range planned to be used for the Phase II proof of concept study, which is expected to start later this year.

Although Addex have described the clinical trials as successful, Phase I clinical trials do not involve people with the medical disorder. So nobody with Parkinson's Disease was actually involved in the clinical trial. For the full details go to the Press release. Excessive dopamine can lead to dyskinesia, and is usually caused by taking too much L-dopa. Therefore, keeping L-dopa to sufficient rather than excessive dosages can help to reduce dyskinesia.

 

30th January 2009 - New research

OMEGA-3 FATTY ACIDS REDUCE DEPRESSION IN PARKINSON'S DISEASE

Journal of Affective Disorders [2008] 111 (2-3) :351-359 (da Silva TM, Munhoz RP, Alvarez C, Naliwaiko K, Kiss A, Andreatini R, Ferraz AC.) Complete abstract

Omega-3 fatty acids are fatty acids that have numerous functions in the body, and that the body can not make itself. They are therefore like vitamins in that they must be obtained in the diet or in dietary supplements. Rapeseed oil (canola oil), which is used for frying and in salads is a commonly available source. One of the richest sources is fish oil. For more information go to Omega-3 fatty acids.

The effect of fish oil supplements was assessed for the first time in people with Parkinson's Disease who suffered from serious depression. Patients were given fish oil (containing omega-3 fatty acids) for three months and were matched against a placebo group. On two of the three depression scales used, patients taking omega-3 fatty acids significantly reduced their depression. Omega-3 fatty acid levels in their body also increased in response to the supplements. The study does not state the means by which the Omega-3 fatty acids helped to reduce depression. Omega-3 fatty acids are not directly involved in forming dopamine. They probably act by forming prostaglandins, which are hormone like substances that have numerous biological functions.

 

29th January 2009 - New research

EARLY VERSUS DELAYED USE OF RASAGILINE

Movement Disorders [2008] [Epub ahead of print] (Hauser RA, Lew MF, Hurtig HI, Ondo WG, Wojcieszek J, Fitzer-Attas CJ) Complete abstract

Rasagiline is a MAO-B inhibitor. MAO-B inhibitors do not directly increase the formation of dopamine. Instead they increase dopamine levels by reducing its breakdown. The most common MAO-B inhibitors are Selegiline  (Eldepryl) and Rasagiline (Azilect). MAO-B inhibitors cause widespread side effects. The purpose of this study, involving over 400 patients, was to assess whether it was better to begin the use of Rasagiline in Parkinson's Disease early, or whether it was better to delay its use.

Those patients that began Rasagiline earlier were found to have lesser symptoms after every one of the time periods that was assessed (from six months to longer than five years). However, The study does not appear to have assessed whether worse side effects were experienced due to beginning Rasagiline earlier, or if higher dosages of Rasagiline were eventually needed in order to sustain the better effects seen due to starting Rasagiline earlier.

 

28th January 2009 - New research

PARKINSON'S DISEASE IN TWINS

Neurobiology of Aging [2008] 29 (12) : 1765-1773 (Wirdefeldt K, Gatz M, Bakaysa SL, Fiske A, Flensburg M, Petzinger GM, Widner H, Lew MF, Welsh M, Pedersen NL.)  Complete abstract

It is claimed by some people that Parkinson's Disease is genetic - not merely that genetic mutations can lead to Parkinson's Disease in some people, which does occur, but that Parkinson's Disease occurs far more commonly when somebody has a close relative who has Parkinson's Disease. Genetically, twins are the closest of all relatives. This study assessed how commonly Parkinson's Disease occurred in both twins. Nearly 50,000 twins were assessed. Out of those, 132 people were found to have Parkinson's Disease. Over 7% of cases reported a first degree relative with Parkinson's Disease.

However, only three of those people with Parkinson's Disease were found to be pairs of twins. This made the likelihood of both twins developing Parkinson's Disease very small. It completely contradicts the notion that Parkinson's Disease occurs far more commonly amongst close relatives. Besides relatives passing on their genes, they often pass on aspects of their lifestyle. Lifestyle similarities rather than genetics would better explain more than one person within the same family having Parkinson's Disease.

 

26th January 2009 - New clinical trial

NEW CLINICAL TRIAL OF GENE THERAPY

The primary fault in Parkinson's Disease is the insufficient formation of dopamine. It has been claimed that, in Parkinson's Disease, there is also insufficient formation of GABA. Both dopamine and GABA are involved in muscular movement. However, increasing dopamine formation or activity, by various means, has always proven to be the most effective method of treatment. Neurologix believe that increasing the formation of GABA may be a more effective approach. For more information go to the News release.

Neurologix are to carry out a clinical trial using a gene therapy that aims at increasing the formation of GABA.  They intend doing this by increasing the quantity of GAD (Glutamic Acid Decarboxylase). GAD is what the brain uses naturally in order to make GABA. Participants will receive an infusion of the gene-based treatment via a catheter temporarily placed in their subthalamic nucleus. This part of the brain is the main surgical target in treating Parkinson's disease. For the full details of the clinical trial go to the Clinical trial study.

GDNF was a previous method of using gene therapy in Parkinson's Disease. However, although claimed as curative by some, in large scale clinical trials it was shown to have no effect at all in ridding Parkinson's Disease. There is no evidence that reduced GABA formation causes Parkinson's Disease anyway. Instead, reduced GABA is sometimes merely associated with Parkinson's Disease. The formation of  GABA can be increased more readily by taking the supplements glutamic acid and pyridoxine (vitamin B6), because these are what GABA is made from.

 

25th January 2009 - New clinical trial

CLINICAL TRIAL OF COENZYME Q10

A large new clinical trial involving 600 patients is being arranged in order to assess the efficacy of Coenzyme Q10 in Parkinson's Disease. Patients are still able to enrol in the clinical trial. For the full details go to the Clinical trial study. Coenzyme Q10 is essential for the proper functioning of the mitochondria.

The mitochondria is the energy producing part of cells. Coenzyme Q10 can also act as an anti-oxidant, and is consequently claimed to reduce cell damage. Coenzyme Q10 is a supplement rather than a drug. It is widely used as a supplement in Parkinson's Disease because it is suggested that the mitochondria and energy production is deficient in Parkinson's Disease. However, Coenzyme Q10 does not, even in theory, address the primary fault in Parkinson's Disease, which is the insufficient formation of dopamine. This may be why in the last major clinical trial of Coenzyme Q10, Coenzyme Q10 was found to have no effect at all in Parkinson's Disease. For the details of that study go to the Complete abstract. In the past few years, the enthusiasm for the use of Coenzyme Q10 has declined.

 

23rd January 2009 - New research

HEAD INJURY AS A CAUSE OF PARKINSON'S DISEASE

BMJ [2008] 337 : a2494 (Rugbjerg K, Ritz B, Korbo L, Martinussen N, Olsen JH.)
Complete study

Head injury is often claimed as a cause of initiating symptoms of Parkinson's Disease. Researchers assessed the prevalence of head injury in people with Parkinson's Disease in comparison to other people of a comparable age and gender. People were assessed for their hospital visits for head injuries. This is the largest study there has ever been of this kind.

There was a 50% increase in the prevalence of hospital visits for head injury in people with Parkinson's Disease. However, this linking of head injury and Parkinson's Disease was only found when the head injuries occurred in the three month period before Parkinson's Disease symptoms first occurred. The link between head injuries and Parkinson's Disease during this period steeply increased. However, head injuries four months or longer before symptoms first occurred were found to be largely unrelated to initiating Parkinson's Disease. Head injuries years before symptoms began were found to be of little significance.

Severe head injuries make Parkinson's Disease even more likely, except when those injuries are caused by fractured skulls or intracranial haemorrhage. The authors suggest that the effect of head injury on Parkinson's Disease must be rapid. However, instead of cell death causing symptoms, they suggest that head injuries damage the blood-brain barrier, thereby exposing the brain to various damaging factors.

 

17th January 2009 - New research

THE CARERS VERY DIFFERENT VIEW OF PARKINSON'S DISEASE SYMPTOMS

Aging and Mental Health [2008] 12 (5): 647-653 (McKinlay A, Grace RC, Dalrymple-Alford JC, Anderson TJ, Fink J, Roger D.) Complete abstract

This study examined the level of agreement between carers and Parkinson's Disease patient reports of neuropsychiatric problems. An equal number of patients and people that knew the patient well were questioned using commonly used questionnaires concerning depression, apathy, anxiety, and Parkinson's Disease.

The level of agreement between the two groups was very low, with only 46% agreement for depression, 45% for apathy, 29% for hallucinations, 27% for sleep problems and 7% for anxiety. Given this low level of agreement between self and other report, these two methods of assessment cannot be considered interchangeable. It really does matter whether or not it is the patient or the relative or carer who answers questions concerning a person's symptoms, because they have very different perceptions of them.

 

16th January 2009 - New research

loss of sense of smell in parkinson's disease

Parkinsonism Related Disorders [2009] Jan 10. [Epub ahead of print] (Haehner A, Boesveldt S, Berendse HW, Mackay-Sim A, Fleischmann J, Silburn PA, Johnston AN, Mellick GD, Herting B, Reichmann H, Hummel T.) Complete abstract

Reduced sense of smell is a well established symptom of Parkinson's Disease. The number of people with Parkinson's Disease that were thought to be affected in this way has ranged from 45% to 90%. The present study was the largest of its kind, assessing 400 patients in three different countries. They used "Sniffin' Sticks" to assess patients, who underwent a psychophysical olfactory test that is comprised of 3 subtests of olfactory function. Out of the total number of patients, 45% were found to have anosmia (a complete loss of sense of smell). Nearly 52% were found to have hyposmia (a greatly reduced sense of smell). Only 3% of people with Parkinson's Disease (a mere 1 in 33) had a normal sense of smell. This means that a greatly reduced sense of smell in Parkinson's Disease is far more common than tremor, which occurs in only 70% of people with Parkinson's Disease.

Substances commonly used to assess the sense of smell are fresh coffee, lemons, garlic, cinnamon. If somebody can not smell them at at all they have anosmia. If they can be smelt, but only mildly, somebody would have hyposmia. If the smell of any of these is very strong, then somebody's sense of smell is fully functional.

 

14th January 2009 - News release

michael j.fox foundation funds six new approaches

The Michael J.Fox Foundation is funding six new approaches for Parkinson's Disease. Two of the projects are assessing the effects of drugs that are normally used for other medical disorders. One team will investigate the potential of Simvastatin (a drug currently used to treat high cholesterol) to reduce dyskinesia in Parkinson's Disease. For more information go to the full details. Another team will assess the effect of Isradipine (a drug for high blood pressure) in its ability to relieve dopamine producing neurons from degeneration that occurs in Parkinsonís Disease. For more information go to the full details. The biochemistry of these two drugs is completely unrelated to Parkinson's Disease. The Foundation does admit that these approaches seem irrelevant to Parkinson's Disease, but claim that preclinical studies suggest that they might be beneficial.

The Foundation is funding four other projects, including three new types of drug. For more information go to the full details. One of them aims to show that "cerebrospinal fluid based biomarkers measuring microtubule-mediated transport of cargo molecules in neurons are altered in people with Parkinsonís disease." This study is very remote from the known biochemistry of Parkinson's Disease, and so does not have the potential to result in anything of practical significance. Funding is also being provided for three new types of drugs : ER-beta selective agonists, type 7 phosphodiesterase (PDE7) inhibitors, and Multiphosphatase Inhibitors. The primary fault in Parkinson's Disease is known to be insufficient dopamine formation. Yet none of these three drugs, even in theory, has the potential to increase dopamine formation.

The front page of the Michael J.Fox Foundation web site claims "We don't just fund research. We fund results." However, despite their good intentions, none of their numerous projects have ever resulted in anyone ever being rid of Parkinson's Disease. This is largely because of the faulty scientific basis on which their projects have been based.

 

10th January 2009 - New research

using lasers with Parkinson's Disease

Journal of Biological Chemistry [2009] 284 (2) : 1009-1017 (Ozawa D, Yagi H, Ban T, Kameda A, Kawakami T, Naiki H, Goto Y.) Complete abstract

Alpha-synuclein is an element in the cells whose accumulation and toxic effects have been claimed to be a cause of Parkinson's Disease. For more information go to Alpha-Synuclein. Researchers have been observing the formation of amyloid proteins - a group of substances that includes alpha-synuclein - using a fluorescence dye that is specific for amyloid. They found that a technique used to visualize amyloid under experimental conditions, might also have clinical potential. The same lasers would be used to destroy the amyloid proteins by inhibiting their growth and degrading them. They found that under the right conditions, the laser could actually stop amyloid fiber growth and even degrade the amyloids. Click here for more details and a video.

There are people with Parkinson's Disease that have no accumulation of alpha-synuclein, and people who have accumulated alpha-synuclein who do not have Parkinson's Disease. So ridding alpha-synuclein does not mean ridding Parkinson's Disease. Alpha-synuclein is a damaging element of cells that appears to be as a result of Parkinson's Disease rather than a cause of Parkinson's Disease.

 

7th January 2009 - New research

the assessment of deep brain surgery for Parkinson's Disease

The Journal of the American Medical Association [2009] 301 (1) : 63-73 Frances M. Weaver, Kenneth Follett, Matthew Stern, Kwan Hur, Crystal Harris, William J. Marks Jr, Johannes Rothlind, Oren Sagher, Domenic Reda, Claudia S. Moy, Rajesh Pahwa, Kim Burchiel, Penelope Hogarth, Eugene C. Lai, John E. Duda, Kathryn Holloway, Ali Samii, Stacy Horn, Jeff Bronstein, Gatana Stoner, Jill Heemskerk, Grant D. Huang) Complete abstract

Deep brain stimulation (DBS) is a method of treatment for advanced 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. For more information go to Deep brain stimulation. There were few randomized clinical trials comparing treatments, and most of those studies did not include older patients.

Consequently, researchers compared the use of DBS with the best medical alternatives. Patients who were using DBS gained an average of 4.6 hours "on" time without it causing dyskinesia. Movement symptoms improved in more people using DBS - 71% of them in comparison to 32% that were not using DBS. Those people using DBS experienced significant improvements in the quality of life. However, patients using DBS had nearly 4 times the risk of experiencing a serious adverse event. The most common serious adverse event was surgical site infection, with other serious adverse events including nervous system disorders, psychiatric disorders, device-related complications and cardiac disorders.

 

3rd January 2009 - New research

the overdiagnosis of Parkinson's Disease

Movement Disorders 2008 Dec 31; [Epub ahead of print] (Marshall VL, Reininger CB, Marquardt M, Patterson J, Hadley DM, Oertel WH, Benamer HT, Kemp P, Burn D, Tolosa E, Kulisevsky J, Cunha L, Costa D, Booij J, Tatsch K, Chaudhuri KR, Ulm G, Pogarell O, Hoffken H, Gerstner A, Grosset DG.) Complete abstract

Faulty diagnosis of Parkinson's Disease is a frequent problem. The textbook descriptions of Parkinson's Disease are not what is commonly seen in practice, because people with Parkinson's Disease can differ considerably regarding their symptoms. In a European study, people taking part in clinical trials who had been diagnosed with early Parkinson's Disease had their clinical diagnosis compared with the results from an assessment using SPECT imaging. SPECT imaging can give a near certainty of diagnosis that is far more reliable than a diagnosis based on questions and observations. Up to 15% of patients were found to have been wrongly diagnosed with Parkinson's Disease. In the U.S.A. misdiagnosis of Parkinson's Disease is even more common, with up to 25% of people who are diagnosed with Parkinson's Disease not actually having it.

Tremor is often wrongly assumed to indicate Parkinson's Disease, even though around 30% of people with Parkinson's Disease don't have tremor. Tremor occurs in a diversity of medical conditions that have nothing to do with Parkinson's Disease. Faulty diagnosis can also occur because there are other medical disorders whose symptoms overlap with those of Parkinson's Disease. For more information go to Parkinsonism.

Most drugs used to treat Parkinson's Disease can cause an after effect that simulate Parkinson's Disease to such an extent that Parkinson's Disease drugs can end up being the primary cause of Parkinson's Disease symptoms. So somebody who is wrongly diagnosed with Parkinson's Disease can end up with Parkinson's Disease symptoms because of the same drugs that are aimed at ridding a medical disorder that they did not actually have to begin with.

 

2nd January 2009 - New book

Therapeutics of Parkinson's Disease and Other Movement Disorders

Mark Hallet (Editor), Werner Poewe (Co-Editor)

Publisher's description : Provides a comprehensive update on therapies for Parkinsonís disease and other movement disorders. Describes the basic mechanisms of neurodegeneration, pharmacologic interventions for motor and non-motor symptoms, and surgical management. Features summary tables and algorithms that serve as a quick reference guide for practical treatment decisions. This is the only current book on movement disorders to emphasize treatment. The authors, experts in their field, have used evidence from randomized controlled clinical trials to develop practical recommendations for every day clinical practice, bringing their personal clinical acumen and therapeutic wisdom to the book. Click here for more details.

 

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