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30th November 2007 : New research

the prevalence of dyskinesia

Neuroepidemiology [2007] 29 (3-4) : 163-169 [Epub ahead of print] (Woitalla D, Mueller T, Russ H, Hock K, Haeger DA.) Complete abstract

Dyskinesia, often occurring as jerky movements of the arms or head, can occur in Parkinson's disease after several years of dopaminergic treaments. Many Parkinson's disease patients treated with dopaminergic drugs develop motor fluctuations and/or dyskinesia.

This large, retrospective study was conducted to compare the prevalence and treatment of dyskinesia in seven countries. A third of people with Parkinson's Disease were found to have dyskinesia, making it more common than was previously assumed. The overall prevalence was 34%. However, the rate varied according to geographical location from 24% to 51%. Regardless of geographical location, physicians were dissatisfied with the current treatment strategies for dyskinesia.


28th November 2007 : News report

claimed breakthrough using gene therapy

The world's first gene therapy for a brain disease brought about significant improvements in the mobility of Parkinson's sufferers. American doctors claimed it could also herald a landmark in the treatment of other neurological disorders. However, there was a lingering doubt that the reports by a dozen patients of improvements of up to 65% in mobility could be anecdotal or due to the placebo effect. The average effect was only a 30% improvement.

Copies of the human gene used in the therapy were grown in bacteria from DNA isolated from a human sample and the gene multiplied with the bacteria for the treatment. The gene was packaged in a virus and patients were given injections of billions of copies of the genetically altered viruses into the brain. The genes are for an enzyme called glutamic acid decarboxylase, whose sole function is the formation of GABA. GABA is a substance in the brain involved in the control of muscular movement. For more information go to the Complete article.


27th November 2007 : New research

fatty acids lessen toxic damage in parkinson's disease

FASEB Journal [2007] Nov 21; [Epub ahead of print] (Bousquet M, Saint-Pierre M, Julien C, Salem N Jr, Cicchetti F, Calon F) Complete abstract

In this study, researchers examined whether omega-3 (n-3) polyunsaturated fatty acids (PUFAs) may exert neuroprotective action in Parkinson's disease, as was previously shown in Alzheimer's disease. Low dietary consumption of omega-3 fatty acids is already associated with a higher risk of neurodegenerative diseases. Mice were exposed to MPTP, which is a toxin known to cause Parkinson's Disease.

However, those mice that were also given the fatty acids did not lose their dopamine producing cells, as did those mice that didn't consume fatty acids, suggesting that the fatty acids offered protection from the toxic damage caused by MPTP. Cooking oils and fats are made up of fatty acids. Some of these fatty acids are just like vitamins in that they are essential for important biochemical functions in the body. Because humans they can not make their own they have to be consumed in the diet. The highest source of these fatty acids is rapeseed oil (canola oil) and to a lesser extent, olive oil. Somebody can greatly increase their intake of these essential fatty acids merely by using these oils for cooking and in salads instead of other oils and fats.


26th November 2007 : New research

smoking lessens the likelihood of tremor

Movement Disorders [2007] Nov 12; [Epub ahead of print] (Benito-Leon J, Louis ED, Bermejo-Pareja F) Complete abstract

People that had ever smoked were found to be marginally less likely to suffer from tremor than people that had never smoked at all. Regular smokers were found to be far less prone to tremor that non-smokers. This lower likelihood of tremor escalated in proportion to the amount of cigarettes smoked and the number of years that somebody had smoked for. Basically the more somebody had smoked the less likely they were to suffer from tremor.


25th November 2007 : News report

claim that stem cells will rid parkinson's disease in five years

Stem cell therapy will be utilized in treating patients suffering from Parkinson's disease within the next five years, claimed Olle Lindvall, a professor of Lund University in Sweden.

He said that the cure for the Parkinson's disease is likely to be one of the first and most effective applications of human stem cell research, though the field in general has many obstacles to overcome. "I think that Parkinson's disease is one of the diseases where we will be able to do the first clinical test,'' Lindvall told The Korea Times. "With the stem cell approach, though I cannot guarantee, scientifically-based clinical trials will be carried out within five years. When it comes to the other diseases, it is less sure.'' For more information go to the Complete article.

The problem with his claims is that in China, Americans and Europeans have already had stem cell implants, yet they all still have Parkinson's Disease. During the contentious debates over the use of stem cells in Parkinson's Disease there was such a preoccupation with the ethical issues that the issue of whether it was actually scientifically sound were largely overlooked. The use of stem cells in Parkinson's Disease is based on the assumption that there is massive cell loss in Parkinson's Disease, and that the cells therefore need replacing. However, not a single study has ever shown that there is massive cell loss in Parkinson's Disease. Given that the theoretical basis of stem cell use is based on a fallacy, it is not surprising that the use of stem cells has already been shown in practice not to rid Parkinson's Disease.

                                                                                                                                                                                  14th November 2007 : New research


Movement Disorders [2007] Nov 6; [Epub ahead of print] (Reijnders JS, Ehrt U, Weber WE, Aarsland D, Leentjens AF.) Complete abstract

Prevalence rates of depressive disorders in Parkinson's Disease vary widely across studies, ranging from less than 3% to more than 90%. The aim of this review was to assess the prevalence of depression in Parkinson's Disease
taking into account the different means of assessment.

Over 100 articles were assessed for quality. Nearly 40% of people with Parkinson's Disease were found to suffer from depression. Nearly half of these suffered from severe depression.  There were an additional 13% that suffered from dysthymia, which is less disabling but longer lasting. Other methods of assessment found lower percentages. This review suggests that depression is common in Parkinson's Disease, but less than previously assumed,  because half of people with Parkinson's Disease are not really affected by it.


13th November 2007 : New research


Movement Disorders [2007] Nov 6; [Epub ahead of print] (Sung YH, Chung SJ, Kim SR, Lee MC.) Complete abstract

Researchers aimed to evaluate the clinical factors predicting a response to dopaminergic treatment for resting tremor in people with Parkinson's Disease.

Although it is often assumed that tremor will respond to dopaminergic treatments if it is due to Parkinson's Disease, only 42% were responsive. The majority (58%) of those with resting tremor were not responsive to dopaminergic treatments. Those that were responsive scored higher for Parkinson's Disease, rigidity, bradykinesia, and postural impairment. These results suggest the possibility that some people with Parkinson's Disease have resting tremor that is not due to Parkinson's Disease at all.


12th November 2007 : New research


Movement Disorders [2007] Nov 6; [Epub ahead of print] (Powers KM, Kay DM, Factor SA, Zabetian CP, Higgins DS, Samii A, Nutt JG, Griffith A, Leis B, Roberts JW, Martinez ED, Montimurro JS, Checkoway H, Payami H.) Complete abstract

Inverse associations of Parkinson's Disease with cigarette smoking, coffee drinking, and non-steroidal anti-inflammatory drug (NSAID) use have been reported individually, but their joint effects have not been examined. A study was conducted that assessed their combined effect. Smoking, coffee, and over the counter NSAID use as individual factors exhibited reduced the risk by between 20% and 30%. Using two of these reduced the risk by even more - between 37% and 49%. However, using all three together caused the risk of Parkinson's Disease to reduce even further, by 62%. People that smoked the most cigarettes, drank the most coffee and took NSAIDs reduced the risk of Parkinson's Disease even beyond that, by 87%. Rather than reduce the risk of Parkinson's Disease would these unhealthy ways even reduce Parkinson's Disease itself  ?  


11th November 2007 : News report


It is claimed that a cough suppressant and a drug tested as a schizophrenia therapy could curb dyskinesia - the involuntary movements that are the disabling side effects of taking the Parkinson's Disease medication L-dopa. Dextromethorphan, used in cold and flu medications as Robitussin, Sucrets, Triaminic and Vicks, suppresses dyskinesia in rats.

The researchers also found that BMY-14802, a drug previously tested in people with schizophrenia suppressed dyskinesia in rats more effectively than dextromethorphan did, suggesting that BMY-14802 might work to block dyskinesia in people with Parkinson's Disease. "These results were unexpected, but very exciting," claimed the study's lead author. "We have filed a patent for the use of BMY-14802 for dyskinesias and we hope to get funding to begin human trials very soon." For more information go to the Complete article. Santhera are about to assess JP-1730a a completely different and more extensively assessed drug for dyskinesia. For more information go to the Complete article.

Despite this being widely reported, the scientific and experimental evidence on which these claims are based is very weak. It has never been tested in anybody or in Parkinson's Disease. Even the rats they tested did not have Parkinson's Disease. Dyskinesias are normally caused by the excessive effects of dopamine. By using an anti-schizophrenic drug they could lower dopamine activity, and could thereby reduce dyskinesia. However, they can also inadvertently cause Parkinson's Disease symptoms as a result of doing this. As the rats did not have Parkinson's Disease they could not be evaluated for the excessive effect that an anti-schizophrenic drug would have.


10th November 2007 : New research

the Parkinsonian heart

Current Medicinal Chemistry [2007] 14 (23) : 2421-2428 (Fornai F, Ruffoli R, Soldani P, Ruggieri S, Paparelli A.) Complete abstract

In Parkinson's Disease there is, over time, progressively greater involvement of different regions of the nervous system. This occurs simultaneously with the specific loss of sympathetic cardiac axon terminals. This causes a cardiovascular dysfunction, which occurs solely in people with Parkinson's Disease, that the researchers describe as
"Parkinsonian Heart".

Parrkinsonian Heart is characterized by a severe loss of the physiological noradrenergic innervation and a slight impairment of central autonomic control. Both of these prevent the heart's proper functioning. It is often characterized by drug-induced physical and functional alterations. Dopamine agonists - which are commonly used in Parkinson's Disease - could make an already abnormal heart even worse. In people with Parkinson's Disease, dopamine agonists, that are of the type ergot derivatives, may frequently produce valvular fibrosis, which is the formation of excessive fibrous connective tissue in the valves of the heart that restrict the heart's function. These effects recently became a major issue, and led to the consideration of all ergot dopamine agonists as dangerous for the treatment of Parkinson's Disease.


9th November 2007 : New research


Parkinsonism and related disorders [2007] (Kim HJ, Kim JY, Ha Paek S, Jeon BS.) Complete abstract

Generally, symptoms of Parkinson Disease patients become worse as L-dopa wears off. However, recently, four Parkinson's Disease patients reported that their motor functions get better after L-dopa wears off. These patients were admitted and their pattern of motor fluctuations was monitored. All four showed a novel pattern where motor function spontaneously got better near to their  "on" level without medication after the effect of L-dopa wore off.

In a way this is not surprising. The primary fault in Parkinson's Disease is that people are not forming sufficient quantities of L-dopa. When people with Parkinson's Disease take L-dopa, it supplies the L-dopa that they need, but it also (by a process called feedback inhibition) reduces their ability to produce their own L-dopa. So the more L-dopa somebody takes, the less they'll make. L-dopa is consequently also a cause of Parkinson's Disease symptoms. Although somebody may have needed to take L-dopa at some point in their life, taking L-dopa perpetuates that need, sometimes well after the original cause of their need has gone.


8th November 2007 : New research

NSAIDS such as aspirin reduce the risk of Parkinson's disease

Neurology [2007] 69 (19) : 1836-1842 (Wahner AD, Bronstein JM, Bordelon YM, Ritz B.) Complete abstract

Researchers have claimed that over-the-counter pain medications, known as non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, may reduce the risk of Parkinson's Disease. Markers of neuroinflammation have been observed in the brains and cerebrospinal fluid of patients with Parkinson disease. Yet the link between anti-inflammatory drugs and Parkinson's Disease remains uncertain.

Researchers studied NSAID use among people with Parkinson's Disease. Their data suggested that the risk of Parkinson's Disease was halved among regular aspirin NSAID users. By regular, they mean 2 or more pills per week. The risk of Parkinson's Disease was reduced even more to just over a third for regular non-aspirin NSAID users, particularly those who reported two or more years of use. The aspirin effect differed by gender, showing a beneficial effect only in women, especially regular users. Previous research also showed a reduced risk, but only down to around two thirds, and only with the use of Ibuprofen. For more information go to the Complete abstract

Reducing inflammation also greatly improves the blood flow to the brain, and thereby increases the supply of those substances to the brain that are needed to form dopamine. So rather than this study being evidence that Parkinson's Disease is due to inflammation, anti-inflammatory drugs may be having only an indirect benefit in Parkinson's Disease by indirectly increasing dopamine formation. This would explain why, according to the earlier study, their beneficial effects are quite moderate.


7th November 2007 : New research

mineral levels in people with Parkinson's disease

Journal of Trace Elements in Medicine and Biology [2007] 21 (4) : 234-241 (Alimonti A, Bocca B, Pino A, Ruggieri F, Forte G, Sancesario G.) Complete abstract

To ascertain the potential role of chemical elements (namely, Aluminium, Barium, Beryllium, Bismuth, Calcium, Cadmium, Cobalt, Chromium, Copper, Iron, Lithium, Magnesium, Manganese, Molybdenum, Nickel, Lead,
Silicon, Tin, Strontium, Thallium, Vanadium, Tungsten, Zinc and Zirconium) as markers in Parkinson's disease, the concentrations of these elements in the cerebrospinal fluid of patients with Parkinson's Disease was assessed. Cerebrospinal fluid is the fluid around the brain. Significantly lower levels of Cobalt, Chromium, Iron, Lead, Silicon and Strontium were observed in the cerebrospinal fluid of people with Parkinson's Disease patients when compared with those in controls.

No variations were detected for all the other elements. Results suggested that Lead, Chromium, and Iron were the most suitable elements to distinguish  people with Parkinson's Disease. This tends to nullify claims that Parkinson's Disease is normally due to the toxicity of one or more of these substances, because none were found to be present in high levels in Parkinson's Disease. It is not surprising that iron levels were found to be low, because iron is essential for the formation of L-dopa - which is the primary biochemical fault in Parkinson's Disease. Chromium levels being low is more surprising because Chromium levels are usually low in Diabetes rather than Parkinson's Disease due to Chromium being essential for the function of insulin.


6th November 2007 : New book

SURVIVING ADVERSITY : living with Parkinsonís disease

Gord Carley

Surviving Adversity - living with Parkinson's disease contains twenty eight profiles of individuals who share their stories of how they have adjusted to having Parkinsonís disease. This book aims to provide readers with perspective and hope. The interviewees' ages range from 29 to 95. They include a professional golfer, a neurologist, an acclaimed lawyer, a childrenís author, a nurse, a legendary cyclist, a former Attorney General, a highly respected news anchor and twenty other men and women. The link to the table of contents on the left hand of their web site details the names of the people that are the subject of the chapters. Fifty per cent of the net proceeds from the book are allocated for Parkinson's Disease. Click here for more details


5th November 2007 : New research

high Prevalence of speech difficulties in Parkinson's disease

Journal of Neurology, Neurosurgery and Psychiatry [2007] 78 (11) : 1188-1190 (Miller N, Allcock L, Jones D, Noble E, Hildreth AJ, Burn DJ.) Complete abstract

Speech difficulties, such as unclear or slurred speech (dysarthria), become inevitable in Parkinson's disease due to the effect of Parkinson's Disease on the muscles involved in speech. Researchers aimed to establish the prevalence of impaired speech intelligibility in people with Parkinson's Disease and the relationship of the decline to indicators of Parkinson's Disease
progression. Nearly 40% of patients placed speech changes among their top four concerns regarding Parkinson's Disease.

The speech of around 70% of people with Parkinson's Disease was found to be affected, making it one of the most common problems. The intelligibility of speech in people with Parkinson's Disease was not related to age or disease duration. It was only weakly related to the stage and the severity of Parkinson's Disease. There were no significant differences between those that were tremor dominant and those with postural and walking problems.


4th November 2007 : New research

Cognitive decline followS deep brain stimulation (DBS)

Journal of Neurology, Neurosurgery and Psychiatry [2007] Oct 26; [Epub ahead of print] (York MK, Dulay M, Macias A, Levin H, Grossman R, Simpson R, Jankovic J.) Complete abstract

Researchers investigated the cognitive and psychiatric outcome six months after Deep brain stimulation (DBS) for the treatment of Parkinson's Disease.
DBS is a method of reducing symptoms that uses electrodes implanted into the brain. For more information go to Deep Brain Stimulation. DBS patients were compared to medically-treated Parkinson's Disease patients. The DBS patients demonstrated a significant decline in verbal memory, oral information processing, including verbal fluency, and word naming.

DBS patients also demonstrated a decline in attention, but this was no different from those that had not had DBS.  DBS patients did not demonstrate significant changes in depression, anxiety, or psychological distress scores.


3rd November 2007 : New research

serious decline in driving ability in Parkinson's Disease

Brain [2007] 130 (Pt 9) : 2433-2440 (Uc EY, Rizzo M, Anderson SW, Sparks JD, Rodnitzky RL, Dawson JD.) Complete abstract

Navigating a new route whilst driving uses the driver's cognitive resources and has the potential to impair driving ability in people with Parkinson's disease. The aim of this study was to assess navigation and safety errors during a route following task in drivers with Parkinson's Disease. Drivers with Parkinson's Disease performed significantly worse on cognitive, visual and motor tests compared to controls, and took longer to finish the task. People with Parkinson's Disease were more than twice as likely to make incorrect turns, and were nearly twice as likely to commit safety errors. Those most affected were not those with the worst physical movement and physical difficulties, but were those with the worst cognitive function.  


2nd November 2007 : History

Seventeenth century treatment of parkinson's disease

Nicholas Culpeper (1616-1654) was an English botanist, herbalist, physician and astrologer. He published books : The English Physitian (1652) and the Complete Herbal (1653).  For more information go to Nicholas Culpepper. The Complete Herbal contains both pharmaceutical and herbal knowledge. During the seventeenth century, symptoms of Parkinson's Disease were known as palsy and tremblings. Among the recommendations in his Complete Herbal, he suggests sage for "sinews, troubled with palsy and cramp". For centuries prior to this, Sage had also been recommended for tremor in the hands. Amongst other plant remedies he suggested for palsy and trembling were bilberries, briony ("English mandrake"), and mistletoe. In the 1696 edition of his Pharmacopoeia Londinensis, a very odd variety of substances were claimed to be useful in the treatment of "palsies", the "dead palsy", and "tremblings". These included the "oil of winged ants", and preparations including earthworms !


1st November 2007 : New research

Chemical That Triggers Parkinson's Disease "Discovered"

Acta neuropathologica [2007] Oct 27; [Epub ahead of print] (Burke WJ, Kumar VB, Pandey N, Panneton WM, Gan Q, Franko MW, O'Dell M, Li SW, Pan Y, Chung HD, Galvin JE.) Complete abstract

Researchers have claimed they have discovered that dopamine itself actually plays a role in destroying the cells that produce it. Dopamine can break down into a highly toxic chemical known as DOPAL (3,4-dihydroxyphenylacetaldehyde). Using test-tube, cell-culture and animal models, researchers claimed that it is DOPAL that causes alpha-synuclein protein in the brain to clump together, which in turn triggers damage of dopamine-producing cells and leads to Parkinson's Disease. "It's actually DOPAL that kicks this whole process off and results in Parkinson's disease" they claim. For more information go to the Complete article.

The weakness in these claims is that they make the false assumption, as many do, that Parkinson's Disease is due entirely to cell damage. The primary fault in Parkinson's Disease has long been shown to be the insufficient formation of dopamine. That is why dopaminergic drugs so readily rid its symptoms. Insufficient formation of dopamine will also lead to cell damage. It is Parkinson's Disease that causes cell damage - not cell damage that causes Parkinson's Disease. For more information go to Biochemistry of Parkinson's Disease.

They did not demonstrate this effect in people with Parkinson's Disease, or even in humans, but instead in rats that did not have Parkinson's Disease. They also used dosages of DOPAL so high that they would not occur in a real life situation in Parkinson's patients. When the subjects, situation and dosages are altered so much from a real life situation, it can not possibly be concluded what occurs in reality.  Dopamine can break down in to DOPAL in the brain, and DOPAL can be damaging. However, when this occurs it was found to result in Autism not Parkinson's Disease. For more information go to DOPAL and autism.



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