PARKINSON'S DISEASE NEWS

 JANUARY 2008

31st January 2008 - New research

strong placebo effect in parkinson's disease

Movement Disorders [2008] Jan 28; [Epub ahead of print] (Goetz CG, Wuu J, McDermott MP, Adler CH, Fahn S, Freed CR, Hauser RA, Olanow WC, Shoulson I, Tandon PK, Leurgans S; Parkinson Study Group.) Complete abstract
                                                                                                                                                                                   When clinical trials are carried out, they are usually compared to the effect on patients of a placebo. Placebos consist of a substance that will have no effect at all. Patients on clinical trials normally know that there is a strong chance that they will be taking a placebo instead of the drug being tested. Researchers examined the effect of placebos in a wide range of Parkinson's Disease clinical trials involving over 800 patients taking only the placebo.

Placebo related improvements occurred in most Parkinson's Disease clinical trials. The effect was similarly distributed across all six months of the follow-up period, despite having taken nothing of any effect. Placebo responses were similarly distributed over early, mid, and late phases of the follow-up period. The overall placebo response was a falsely assumed reduction of  up to 55% of all symptoms in 16% of people taking the placebo. Patients who started with more severe symptoms were most prone to falsely assuming there had been a positive effect, as were those that took part in clinical trials involving surgery.

30th January 2008 - New research

parkinson's disease patients do better without treatment

Journal of Neurology, Neurosurgery and Psychiatry [2008] Jan 25; [Epub ahead of print] (Asimakopoulos P, Caslake R, Harris CE, Gordon JC, Taylor KS, Counsell C.) Complete abstract

Parkinson's Disease drugs become progressively more counterproductive. L-dopa enables patients to form more dopamine, but it also reduces a person's ability to produce their own L-dopa. Dopamine agonists stimulate dopamine receptors, but in time cause dopamine receptors to become less progressively less sensitive. Consequently, it has been debated whether to adopt a "wait and watch" strategy or to initiate drug therapy soon after being diagnosed with Parkinson's Disease.

This research assessed the outcome of the two options. Those patients that started drug treatment within the first year actually had higher symptom scores after two years than those patients that had remained completely untreated. Those that remained untreated also suffered no significant deterioration in their symptoms over the following two years. The researchers consequently suggest that treatment of Parkinson's Disease be delayed after diagnosis.

29th January 2008 - New clinical trial

Nexalin Advanced Therapy for parkinson's disease

Nexalin Advanced Therapy is a technology that uses a mild stimulation of the brain to treat a variety of mood disorders, specifically Anxiety, Depression, and Insomnia. The waveform of Nexalin is administered by placing medical grade conductive pads produced specifically for the Nexalin technology on the forehead and behind each ear, which are connected to the Nexalin device with thin cables.

The patient is placed in a reclining chair for the duration of a treatment session, which typically lasts for approximately forty minutes. For more information go to Nexalin. The disorders usually treated share a similar biochemistry with Parkinson's Disease. People with Parkinson's Disease have gone to the Nexalin Therapy Center in Germany to assess its effects on Parkinson's Disease. They have already started therapy sessions, and are detailing their progress on the Parkinsons Rebels web site. For more information go to ParkinsonsRebels.

28th January 2008 - New blog

THE RESULT OF STEM CELL SURGERY IN CHINA

On 7th January 2008, Linda and John Fratcher arrived in China in order to have stem cell surgery to rid Linda Fratcher's Parkinson's Disease. For years it has been claimed by some that the use of stem cells would be the cure for Parkinson's Disease. In China and elsewhere, due to there being fewer restrictions, stem cell surgery is already being carried out. The stem cell surgery operation on Linda Fratcher has now been completed. However, she still has Parkinson's Disease, and is still having to take Sinemet. They are continuing to detail what happens to her after the operation day by day in a blog titled  "Linda and John in China", which is on the Parkinson's Rebels web site. For more information go to Linda and John in China.

Despite a number of people having undergone stem cell surgery for Parkinson's Disease, nobody has been cured of it. Every patient has returned from stem cell surgery in China with Parkinson's Disease and is still being treated for it. Reductions in patients' Sinemet have often been due to it being replaced by Mucuna Pruriens, which is a natural form of L-dopa. For more information go to Stem cells in China.

27th January 2008 - New research

should l-dopa dose be reduced when switching to stalevo ?

European Journal of Neurology [2008] Jan 22; [Epub ahead of print] Complete abstract

Changing from L-dopa and Carbidopa (as in Sinemet) to Stalevo (L-dopa, Carbidopa, and Entacapone) increases the "on" time and decreases "off" time, but also increases the likelihood of dyskinesia. Therefore a reduction of the total L-dopa seems appropriate. However, this could result in insufficient efficacy. A clinical trial was carried out to determine the best way in terms of efficacy, tolerability and safety of switching from Sinemet to Stalevo (or the equivalent drugs). Two group were assessed - one group taking the same dosage, and another group whose dosage of Sinemet (or the equivalent) was reduced by up to 25%.

No differences in clinical assessment between the two groups were found. This study suggests that switching from Sinemet to Stalevo (or the equivalent drugs) can be done safely with or without reducing the total L-dopa dosage, but in the clinical setting it would be more practical to keep the L-dopa dosage unchanged unless severe dyskinesia is present.

 

26th January 2008 - New research

the mystery of the kii peninsula

Rinsho Shinkeigaku [2007] 47 (11) : 966-969 (Kokubo Y.) Complete abstract  Rinsho Shinkeigaku [2007] 47 (11) 962 -965 (Kuzuhara S.) Complete abstract Rinsho Shinkeigaku [2007] 47 (11) : 695-702 (Kuzuhara S.) Completeabstract

The Kii Peninsula is a remote part of the Japanese coast. On the mountainous Kii Peninsula, especially in the villages of Hohara and Kozagawa, Parkinson's Disease symptoms have almost been the norm, but nobody knows why. The initial symptoms are Parkinsonian gait and amnesia, followed by akinesia, rigidity and occasional tremor. Patients then go on to develop dementia and ALS, which has been known in the area since 1689.

However, in the 1980's, there was a sudden and massive unexplained reduction in the incidence of those that developed ALS. Despite this, in the 1990's, the incidence of Parkinson's Disease symptoms kept on increasing. The incidence of the syndrome is still over 100 times higher than anywhere else in Japan. For reasons unknown, women are affected almost twice as much as men. Family members are often affected simultaneously. Yet gene analyses failed to reveal any gene mutations in those affected. No particular environmental factors have been confirmed either.

25th January 2008 - News report

STALEVO SURPASSES SINEMET IN CLINICAL TRIALS

Sinemet is a combination of L-dopa plus Carbidopa, which prevents L-dopa from breaking down before it reaches the brain. Stalevo is a combination of L-dopa and Carbidopa, and also Entacapone. For more information go to Stalevo. Stalevo also includes Entacapone (a COMT inhibitor) because it prolongs the activity of L-dopa. Novartis carried out a clinical trial on over 400 people with Parkinson's Disease.  The aim of the study was to determine whether treatment with Stalevo provides more effective relief from Parkinson's Disease than the Sinemet combination of L-dopa and Carbidopa.

The clinical trial was carried out for 9 months. The measure of efficacy was the change in scores on the UPDRS, which is the most widely used  Parkinson's Disease symptom questionnaire, as well as changes in scores assessing daily living and motor function in people with Parkinson's Disease. Effectiveness was statistically significant in favour of Stalevo. For more information go to the Complete article. It is believed that Stalevo will eventually replace the common use of Sinemet.

22nd January 2008 - New research

Electromyograph differentiateS between parkinsonian and essential tremor

Journal of Neurology [2008] Jan 22; [Epub ahead of print] (Breit S, Spieker S, Schulz JB, Gasser T.) Complete abstract

A quarter of people with Parkinson's Disease are wrongly diagnosed. Many of them have Essential Tremor instead of Parkinson's Disease. Having tremor often leads to somebody being assumed to have Parkinson's Disease even though nearly a third of people with Parkinson's Disease don't have tremor. The differential diagnosis of tremor is mainly based on clinical criteria. Nevertheless, these criteria are in some cases not sufficient to differentiate between different types of tremor. Long-term use of EMG (Electromyography) has proven to be a reliable method for the quantification of tremors. EMG is performed using an electromyograph, which detects the electrical activity generated by muscle cells when they contract. For more information go to Electromyography.

The aim of this study was to develop a long-term EMG-based analysis procedure that separates parkinsonian tremor from essential tremor. A formula based on three parameters : tremor occurrence, mean tremor frequency and standard deviation of phase was established and predicted the correct diagnosis in 93% of patients. When this method was used with new patients in the early stages of tremor, it yielded a correct diagnosis in 100% of cases, making it a reliable means of differentiating between parkinsonian and essential tremor.

21st January 2008 - New book

Living with Parkinson's Disease

David Belgum (editor)

Publisher's description : Living with Parkinson's Disease explores the disease from a professional point of view and includes short pieces, written primarily by Parkinson's patients, about what it is like to experience the disease. Some of these short pieces are poems and short essays, but all are poignant and of extraordinary use to doctors, patients, researchers, and coping family members. This work also includes more general articles, which relate to a wider perspective than the description of Parkinson's. The two introductory articles are written by doctors and cover the basic description of Parkinson's Disease. This book is a practical reference for all who come in contact with this debilitating and tragic condition.  Click here for more details 

20th January 2008 - New research

BROMOCRIPTINE FAILS TO BENEFIT EARLY PARKINSON'S DISEASE

Cochrane Database Systematic Review [2007] Oct 17 (4) : CD002258 (van Hilten JJ, Ramaker CC, Stowe R, Ives NJ.) Complete abstract; Coochrane Database Systematic Review [2007] Oct 17 (4) : CD003634 (van Hilten JJ, Ramaker CC, Stowe R, Ives NJ.) Complete abstract

Bromocriptine (which is sold as Parlodel) is a dopamine agonist that is used  in the treatment for Parkinson's disease. Early studies suggested that treating patients with bromocriptine before starting L-dopa would delay the onset of side effects such as dyskinesia. For more information go to Bromocriptine. A complete review of the medical literature was carried out in order to assess whether this was true.

When used alongside L-dopa a systematic review revealed no evidence to support the use of bromocriptine and L-dopa as a strategy to prevent or delay the onset of motor complications in Parkinson's Disease. Results showed no evidence of consistent differences between treatment groups concerning the occurrence and severity of motor complications, scores of impairment and disability, or the occurrence of side effects. When used on its own, bromocriptine was found to be marginally beneficial in only one trial. All other trials showed no benefit regarding disability, and no improvement.

19th January 2008 - News report

MICE WITH HUMAN BRAINS FOR PARKINSON'S DISEASE RESEARCH

In Singapore, scientists eager to splice human genes with animal cells are seeking public feedback on the prospect of such controversial research. A consultation paper on its website said the BAC considers human stem cell research to have considerable potential in the treatment of currently incurable diseases, such as Parkinson's disease.

"While there have been significant advances in stem cell science and technology, research involving human-animal combinations is required for further progress," the BAC claimed. Mice with human brain cells could be used as test beds for Parkinson's disease drugs, they said. Singapore has the technology to create these "mixed animals" that can be created by infusing a human nucleus, the cell's nerve centre, with an animal egg or cell, the BAC chairman stated. The research would likely involve small amounts of human genetic tissue combined with distantly related animals such as rats or mice, he said. Websites against such research say scientists would be playing God by creating half-human, half-animal monstrosities. For more information go to the Complete article.

 

18th January 2008 - News report

HUMAN-ANIMAL HYBRIDS TO BE USED FOR PARKINSON'S DISEASE RESEARCH

Human-animal embryos are to be created in the U.K. after scientists won approval for the practice from the Human Fertilisation and Embryology Authority (HFEA). The stem cell biology laboratory at King's College in London will be using them to study neurological diseases such as Parkinson's Disease. The hybrids are created by transferring the nuclei of human cells, such as skin cells, into animal eggs from which almost all the genetic information has been removed.

The resulting embryo contains only a tiny amount of animal DNA (around 0.1%), with the rest human. The embryo would be grown in a lab and within a week would have divided to form a tiny ball of around 200 cells. Scientists believe they could provide an invaluable source of embryonic stem cells for use in research in human diseases. The national director of the Society for the Protection of Unborn Children (SPUC) said: "The HFEA decision represents a disastrous setback for human dignity in Britain. The deliberate blurring of the boundaries between humans and other species is wrong and strikes at the heart of what makes us human."  For more information go to the Complete article.

17th January 2008 - History

USING ELECTRICITY TO TREAT PARKINSON'S DISEASE

Electrotherapy was used to treat Parkinson's Disease for nearly a hundred years. French doctor Guillame Benjamin-Amand Duchenne (1806-1875), popularized the use of electrical means with his 1855 publication "On localized electrification, and on its application to pathology and therapy".  In 1868, he reported a case in which he had cured Parkinson's Disease, which was then known as paralysis agitans, by using electrotherapy.

The following year, Irish physician U.S.L.Butler also claimed that it had cured a patient of Parkinson's Disease. However, William Sanders in 1865, and Hughlings Jackson and William Gowers in 1893, found it to be "useless". Despite this, electrical stimulation in Parkinson’s Disease continued to be used for decades more. In the 1924 edition of his handbook on electrotherapy, Cohn commented that "remarkable results could not be expected", and that what benefits he had seen were largely psychological. In his 1941 review, Critchley warned against using electricity to treat Parkinson's Disease. The demise in the use of electricity was over fifty years before electricity resumed being widely used again in Parkinson's Disease as Deep Brain Stimulation (DBS).

16th January 2008 - New research

PARKINSON'S DISEASE CAUSED BY EATING FLYING FOXES

Life Sciences [2007] Dec 7; [Epub ahead of print] (Karamyan VT, Speth RC.) Complete abstract

It has long been thought that BMAA (beta-methylamino alanine) was a toxic cause of the symptoms of Parkinson's Disease in a complex with other medical disorders. However, there had never been certainty over the sources of BMAA. It was reported to be a toxic component of the cycad flour consumed by the Chamorros on Guam, who were known to be greatly affected. However, this theory lost interest because only a really massive intake of cycad flour was able to cause Parkinson's Disease symptoms.

Due to physical assessments being made, it is now known that toxic quantities of BMAA originate from several other food sources, that include flying foxes. Flying foxes are the largest bats in the world. Their wing span is as wide as a tall man.  Flying foxes were once eaten in large quantities by the Chamorros, who are the worst affected by BMAA. This research paper critically evaluates studies directed at establishing a model of BMAA-induced Parkinson's Disease symptoms and its implications.

14th January 2008 - New research

L-DOPA CAUSES NEURODEGENERATION

Journal of Neuroscience [2008] 28 (2) : 425-433 (Chen L, Ding Y, Cagniard B, Van Laar AD, Mortimer A, Chi W, Hastings TG, Kang UJ, Zhuang X.) Complete abstract

Dopamine is normally produced naturally in the brain from L-tyrosine (L-tyrosine >>> L-dopa >>> dopamine). The brain regulates how much dopamine is produced by this means. However, when somebody takes L-dopa in a drug form, there is no regulation of its use by the brain. L-dopa taken as a drug indiscriminately forms dopamine. Dopamine produced in this way has been considered to be a vulnerability factor and a toxic cause of Parkinson's Disease. The assumed toxicity of dopamine is responsible for the practice of avoiding the use of L-dopa in early Parkinson's Disease.

When the potential harm of dopamine was assessed it was found to cause motor dysfunctions and progressive neurodegeneration within weeks. The neurodegeneration was accompanied by oxidative stress. L-dopa worsened the motor dysfunction  and accelerated neurodegeneration.  The results provide the first evidence that chronic exposure to unregulated dopamine alone is sufficient to cause neurodegeneration. The present study has significant clinical implications, because dopamine replacement therapy is the mainstay of Parkinson's Disease treatment.

13th January 2008 - New research

SELEGILINE FAILS TO INCREASE THE EFFECT OF L-DOPA

Neurology [2008] Jan 9; [Epub ahead of print] (Wahner AD, Bronstein JM, Bordelon YM, Ritz B.) Complete abstract

Most patients taking L-dopa eventually experience deterioration at the end of the L-dopa dosing interval, with "wearing off" and "on-off" fluctuations. Selegiline orally disintegrating tablet (ODT), which is sold as Zelapar, is a MAO-B inhibitor. It was developed in order extend the effect of L-dopa in Parkinson's Disease. A clinical trial was carried out on Selegiline ODT to see if it did actually reduce the "off" time experienced by people taking L-dopa.

However, its effects were found to be no different from the effect of a placebo. So effectively it did not have any of the effect intended for it. Despite this, patients perceived a small improvement when taking Selegiline ODT, and clinicians perceived a strong improvement - even though there was none.  The outcome is consistent with another study whose results showed little change  in "off" time with Selegiline ODT.

12th January 2008 - New research

STATINS REDUCE THE RISK OF PARKINSON'S DISEASE

Neurology [2008] Jan 9; [Epub ahead of print] (Wahner AD, Bronstein JM, Bordelon YM, Ritz B.) Complete abstract

Statins are drugs that lower cholesterol levels. There are a number of statins, each of which has statin as part of their name. For more information go to Statins. The statins are marketed under various names. It has long been considered that statins may reduce Parkinson's Disease. Researchers investigated the association between statin use and Parkinson's Disease.

They observed a higher frequency of statin use amongst people that did not have Parkinson's Disease. There was also a strong relationship between the dose and the likelihood of having Parkinson's Disease. The more somebody took, the less likely they were to have Parkinson's Disease. This was even more true the longer somebody had been using statins. There was a 60% to 70% reduction in the risk of Parkinson's Disease for each statin except pravastatin. The researchers do not know if statins are the direct cause of this greatly reduced proneness to Parkinson's Disease, or by which means they could act.

11th January 2008 - New resource

GOING TO CHINA FOR STEM CELL SURGERY

For years it has been claimed by some that the use of stem cells would be the cure for many medical disorders, including Parkinson's Disease. Especially in the U.S.A., highly contentious debate has taken place concerning the ethics of using stem cells for use in medical treatment.

However, in China, due to there being fewer restrictions, stem cell surgery is already being carried out. Some North Americans and Europeans have already travelled to China for treatment. Americans - Linda and John Fratcher - arrived in China on 7th January 2008 to have  stem cell surgery. They are detailing what happens to them day by day in a blog titled  "Linda and John in China", which is on the Parkinson's Rebels web site. For more information go to Linda and John in China.

10th January 2008 - New research

RASAGILINE (AZILECT)- A COMPREHENSIVE REVIEW

9th January 2008 - New research

THE NUMBER OF ELECTRODES ALTERS THE EFFECT OF DBS SURGERY

Neurosurgery [2007] 61 (5 Suppl 2) : 346-355 (Temel Y, Wilbrink P, Duits A, Boon P, Tromp S, Ackermans L, van Kranen-Mastenbroek V, Weber W, Visser-Vandewalle V.) Complete abstract

DBS is a surgical method of greatly reducing Parkinson's Disease symptoms that uses electrodes implanted into the brain. For more information go to Deep Brain Stimulation. It is still debated to what extent the techniques used affect the outcome of deep brain stimulation (DBS). Identification of the Subthalamic nucleus, which is where the surgery is often completed can be carried out using only one electrode or by using multiple electrodes.

Researchers found that the simultaneous implantation of multiple electrodes does not increase the risk of bleeding or any other major intracranial complication. The use of multiple electrodes also resulted in better motor results when compared with patients who underwent DBS that was guided with a single electrode. There were significantly more improvements in patients' tremor and rigidity, and their symptom scores when using multiple electrodes. However, patients treated with multiple electrodes also showed subtle deterioration in their neuropsychological functions, particularly in memory function.

8th January 2008 - News report

NEW ANTIOXIDANT FOR PARKINSON'S DISEASE

Eucalyptus in Israel are to start producing a new antioxidant called N-acetylcysteine amide (AD4), that can be used in a variety of Neurological disorders in which oxidative stress occurs, including Parkinson's Disease, Alzheimer's Disease and Multiple Sclerosis. Oxidative stress is a process that leads to cell damage and further loss of function in medical disorders such as Parkinson's Disease. Unlike many drugs, AD4 is able to cross the blood brain barrier.

The blood brain barrier is a membrane that usually prevents most substances from gaining access to the brain, and so consequently prevents many substances from having any medical effect. Pre-clinical evidence showed the ability of AD4 to pass the blood brain barrier, to protect cells from oxidative damage, to protect neuronal cells from damage, and to possess low toxicity. It is intended that AD4 be taken alongside other treatments for Parkinson's Disease in order to prevent the cell damage that occurs in Parkinson's Disease. For more information go to the Complete article.

7th January 2008 - News report

SILENCING GENES TO RID PARKINSON'S DISEASE

The Michael J. Fox Foundation has committed up to $3.8 million for the development of a gene silencing therapeutic to treat Parkinson's disease. In people with Parkinson's Disease, alpha-synuclein often accumulates in the affected cells. For more information go to Alpha-synuclein. In some rare forms of Parkinson's Disease, alpha-synuclein has been shown to incline people to develop Parkinson's Disease. It has therefore been suggested that alpha-synuclein is a key feature in causing Parkinson's Disease. So researchers aim to reduce the formation (the expression) of alpa-synuclein.  They will also assess whether this slows the progression of the disorder. No drugs exist that are able to achieve this. So if successful the researchers state that they would then have to develop drugs that were able to reduce the formation of alpa-synuclein. For more information go to the Complete article.

Analysis : Alpha-synuclein is a common cellular symptom of idiopathic Parkinson's Disease and other medical disorders. However, no research has ever shown it to cause idiopathic Parkinson's Disease. Parkinson's Disease has long been known to be primarily due to a lack of dopamine, which is why the dopamine precursor L-dopa can have such a potent effect on ridding the symptoms. For more information go to Biochemistry of Parkinson's Disease. However, restricting the formation of alpha-synuclein would not, even in theory, increase dopamine formation.

4th January 2008 - History

THE MEN THAT PRECEDED JAMES PARKINSON

Parkinson's disease was first formally described in 1817 by a London physician named James Parkinson (1755-1824). Parkinson's Disease was subsequently named after James Parkinson because of his detailed description of the disorder.

However, Francois Boissier de Sauvages de la Croix (1706-1767) had already provided one of the clearest descriptions there had ever been of a Parkinsonism-like condition in 1763, well before James Parkinson. Sauvages de la Croix was a French physician and a botanist. For more information go to Sauvages de la Croix. He spoke of a condition that he named "sclerotyrbe festinans" in which decreased muscular flexibility led to difficulties including the initiation of walking and falling. His observations, along with those of  Jerome David Gaubius (1705-1780) and Franciscus de la Boë (1614-1672) were subsequently cited by James Parkinson, because although none of them described the whole syndrome, they all described aspects of it.

3rd January 2008 - News report

THE CAUSE OF CELL DAMAGE IN Parkinson's Disease

Journal of Clinical Investigation [2008] Jan 2; [Epub ahead of print] (Martinez-Vicente M, Talloczy Z, Kaushik S, Massey AC, Mazzulli J, Mosharov EV, Hodara R, Fredenburg R, Wu DC, Follenzi A, Daue) Complete abstract

Researchers are claiming that a faulty mechanism in autophagy (the way cells recycle damaged components) may considerably worsen cell damage in Parkinson's disease. Autophagy is effectively the process of rubbish removal in the cells. Autophagy puts damaged elements in to lysosomes, which are basically rubbish containers, where the damaged elements are broken down and eliminated.  This rubbish removal process is very important in Parkinson's Disease, because the cells involved in Parkinson's Disease are particularly prone to producing damaging elements.  It is widely believed that the accumulation of alpha-synuclein considerably contributes to cell damage in Parkinson's Disease.

Mutant forms of alpha-synuclein found in some people with Parkinson's Disease are not readily disposed of and prevent the disposal of other unwanted substances. Other modified forms of alpha-synuclein can be found in the brains of all people with Parkinson's Disease. It is proposed that dopamine, which normally relieves Parkinson's Disease, alters alpha-synuclein so that it can not enter the lysosomes (the rubbish containers that would normally get rid of it). This interferes with the removal of other damaging elements. It is suggested that this inability to remove damaged elements explains the excessive cell damage found in most people with Parkinson's disease. For more information go to the Complete article.

2nd January 2008 - New research

The effect of L-dopa on speech

Movement Disorders 2007 Dec 28; [Epub ahead of print] (Ho AK, Bradshaw JL, Iansek R.) Complete abstract

The beneficial effect of L-dopa on muscle control has been well documented. However, its effect on speech has rarely been objectively examined.  Consequently, the existing medical literature remains inconclusive. This paper aims to examine the effect of L-dopa on speech in people with Parkinson's disease. Their results showed that, under the effect of L-dopa there was a consistent tendency for increased loudness and a faster rate of speech. However, this was accompanied by a greater decay in the intensity of the voice. The pitch of the voice was unaffected by L-dopa. The ability to articulate also remained unchanged. L-dopa effectively increased the overall vocal amplitude and tempo, similar to its well-known effect on limb movement. However, the effect on the final acoustic effect of a person's speech may or may not be advantageous, depending on the existing speech profile of  the individual patient.

1st January 2008 - New research

THE genetic CAUSES of parkinson's disease

Acta Pharmacologica Sinica [2008] 29 (1) : 21-34 (Rosner S, Giladi N, Orr-Urtreger A.) Complete study

Findings in the last decade suggest that the contribution of genetic causes of Parkinson's Disease is much greater than was previously believed. Some people have unknowingly been susceptible to Parkinson’s Disease since they were born.  Genetic forms of Parkinson’s Disease account for up to 10% of all cases of Parkinson’s Disease. The frequency is only 1%-3% of cases of late-onset Parkinson’s Disease, but is as much as 20% of young-onset Parkinson’s Disease.

The symptoms of genetic forms of Parkinson’s Disease often appear to be no different from those of idiopathic Parkinson’s Disease. There are consequently many people that have genetic Parkinson's Disease that are completely unaware of it. Genetic Parkinson’s Disease does not normally cause Parkinson’s Disease on its own. In those affected, it is instead believed to be an interaction of genetic and other causes. There are now known to be at least twelve genetic mutations that unequivocally linked to Parkinson’s Disease : PARK 1/4 (SNCA), PARK 2 (Parkin), PARK 3 (gene unknown), PARK 5 (UCH-L1), PARK 6 (PTEN-induced kinase 1 or PINK1), PARK 7 (DJ1), PARK 8 (LRRK2), PARK 9 (ATP13A2), PARK 10 (gene unknown), PARK 11 (gene unknown), PARK 12 (gene unknown), PARK 13 (OMI/HTRA2). Each of these mutations affects a different biochemical function, and greatly differs in frequency in different ethnic groups.