TRANSLATE

Welcome to Our Parkinson's Place


I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please no advertisers. This is a free site for all.
Thank you.


Monday, November 12, 2012

PREVALENCE OF PARKINSON'S DISEASE IN CANADA

 September 13, 2012

Parkinsonism Related Disorders [2012] 18 (4) : 327-331 (Allyson Jones C, Wayne Martin WR, Wieler M, King-Jesso P, Voaklander DC.) 






The prevalence of Parkinson's Disease in Canada has been found to be one of the highest of any country in the world. The study was carried out in British Columbia, Canada. The prevalence rates amongst men were found to be 396-207 per 100,000 for men, and 259 to 127 per 100,000 for women. Combining the figures for both men and women gives figures of around 317 to 167 per 100,00.
These figures are just about higher than those in the U.S.A., which has one of the highest prevalence rates of any country. The only countries with higher prevalence rates than Canada are Albania and Egypt, where the prevalence rates are exceptionally high. The ratio of men to women with Parkinson's Disease in Canada is 1.56. As in most countries in the world, in Canada there are more men than women with Parkinson's Disease.

THE SAFETY AND TOLERABILITY OF NEUPRO

9th September 2012 -
 
Parkinsonism Related Disorders [2012] Sep 3 [Epub ahead of print] (Oertel W, Lewitt P, Giladi N, Ghys L, Grieger F, Boroojerdi B.) 
Although dopamine agonists are sometimes perceived as poorly tolerated by the elderly, there is little clinical evidence to support these concerns. So the safety and tolerability of rotigotine transdermal system have been assessed in four 6-month studies. : two in early Parkinson's Disease and two in advanced Parkinson's Disease.Neupro® (Rotigotine Transdermal System) is a dopamine
For most adverse events no age-related differences in were observed. In early Parkinson's Disease those symptoms more common in those younger than 65 in comparison to those who were 65 were : nausea (38% v 30%) and headache (15% v 9%). In another study, amongst older patients, those symptoms more common in those younger than 75 in comparison to those who were 75 were : nausea (36% v 21%), and dizziness (15% v 28%). In people with advanced Parkinson's Disease it was still the younger patients that more commonly had nausea (24% v 19%). It was only falls that were more common in older patients (13% v 8%). So oddly, the adverse events of this dopamine agonists were generally less rather than greater with age, as if the adverse events were adapted to.

NFL PLAYERS TREBLE THE RISK OF PARKINSON'S DISEASE




 September  2012 - New research
 
Neurology [2012] Sep 5 [Epub ahead of print] (Lehman EJ, Hein MJ, Baron SL, Gersic CM.) 
Players in the NFL ("American" Football's National Football League) were found to have treble the risk of haiving a neurodegenerative disease generally. This included Parkinson's Disease, Alzheimer's Disease and ALS. The figures for Alzheimer's Disease were more than three times more likely, and the figures for ALS were more than four times more likely. The likelihood of developing Parkinson's Disease was less than these. Although the research suggests that concussions and repeated blows to the head are likely to blame for the increased risk, the researcher says multiple studies are needed to definitively blame concussions.

Friday, June 15, 2012

George H.W. Bush can no longer walk on his own: Parkinson's struggle revealed with new HBO documentary

Sarah Rufca
culturemap.com - With a documentary on the life of George H.W. Bush set to air on HBO, friends and family are opening up about the Houstonian and 41st president.

Speaking to Charlie Rose on CBS, son Jeb Bush revealed that his father at 87 year of age can no longer walk on his own, instead relying on a wheelchair and a stroller to get around

"That's hard for a guy who's been so vital and vigorous in life," said Jeb Bush, who also called his father his "hero" and added, "I've never met a man as near perfect as George H.W. Bush."

Bush has been known for his vitality despite his advanced age, famously going skydiving to celebrate turning 75, 80 and 85 years old.

On Good Morning America, documentary producer and Bush family friend Jerry Weintraub said that Bush has struggled increasingly with the symptoms of Parkinson's disease in recent years.

"He's not doing great, he's not terrible but he's not doing great. He's a very active guy and when you get Parkinson's and all of a sudden you're riding around in a wheelchair and this and that and he can't do things for himself . . . it's tough."

The HBO documentary, titled simply 41, features unprecedented access to the former president, filmed over 17 months from September 2009 to February 2011. In his own words, the typically reticent Bush speaks about his life, from childhood summers in Kennebunkport and meeting his wife to his experiences as a naval aviator in World War II to his run as a wildcatter in Texas and his rise to the top of politics.

"It shows him as a man. It's not just a documentary about a president. It's not him making big speeches out there, rallying the troops and so on and so forth, it's about his life and his service," Weintraub said.

41 premieres on June 14, two days after Bush's 88th birthday

Thursday, June 7, 2012

FIRST VACCINE FOR PARKINSON'S DISEASE

7th June 2012 - News release


The first clinical trial for the development of a Parkinson’s Disease vaccine has been started by AFFiRiS AG. The vaccine called PD01A is directed against alpha-Synuclein, a protein considered by AFFiRis to cause the onset and progression of Parkinson's Disease. The vaccination aims to educate the immune system to generate antibodies directed against alpha-Synuclein. They believe that a reduction of the brain’s alpha-Synuclein aggregates will have a beneficial impact on the progress of Parkinson's Disease. PD01A aims to accomplish that by the induction of antibodies that are targeting alpha-Synuclein, in order to neutralize its toxic impact.

The vaccine is currently being tested on people with Parkinson’s Disease in a Phase I trial. The clinical trial is taking place in Vienna and involves up to 32 patients. The primary purpose is to assess the safety and tolerability of PD01A.

The weakness in the theory on which the method is reliant is that a lot of people with Parkinson's Disease do not accumulate alpha-Synuclein. So there is none to get rid of. Most people that have an accumulation of alpha-Synuclein in the brain do not have Parkinson's Disease either, thereby proving that alpha-Synuclein is not the cause of Parkinson's Disease.

Sunday, February 12, 2012

THE EFFECT OF TAI CHI ON PARKINSON'S DISEASE

12th February 2012 - New research



New England Journal of Medicine [2012] 366 (6) : 511-519 (F.Li, P.Harmer, K.Fitzgerald, E.Eckstrom, R.Stock, J.Galver, G.Maddalozzo, S.S.Batya) People with Parkinson's Disease tend to have impaired balance, and an increased risk of falling. A clinical trial assessed the effect of Tai Chi on postural control in Parkinson's Disease. Tai Chi is a traditional Chinese martial art and form of exercise. For more information go to Tai Chi. Participants took part in 60-minute exercise sessions twice weekly for 24 weeks. Although the researchers claimed that Tai Chi performed consistently better than other methods, the improvement was only 5% better than resistance training, and 12% better than stretching exercises. The Tai Chi group performed better than the stretching group in all secondary outcomes and outperformed the resistance-training group in stride length and functional reach. Tai Chi lowered the incidence of falls when compared with stretching exercises but not when compared with resistance training.

Out of the previous studies in the medical literature concerning Tai Chi and Parkinson's Disease, four were either non-randomised or uncontrolled clinical trials. Two failed to show any effect. Only one study showed Tai Chi to be superior to conventional exercise for Parkinson's Disease. So the evidence is insufficient to suggest that Tai Chi is effective in Parkinson's Disease.

DUODENAL L-DOPA CAN CAUSE POLYNEUROPATHY


26th January 2012 - New research


Journal of Neurology [2012] Jan 24 [Epub ahead of print] (Santos-García D, de la Fuente-Fernández R, Valldeoriola F, Palasí A, Carrillo F, Grande M, Mir P, De Fabregues O, Casanova J.)  
Neurology [2011] 77 (22) : 1947-1950 (Y.A.Rajabally, J.Martey)


Reports have emerged describing the occurrence of polyneuropathy related to vitamin B12 deficiency and Guillain-Barré syndrome in people with Parkinson's Disease who are being treated with continuous duodenal L-dopa infusion. Duodenal L-dopa is administered as a gel throughout the day using a portable pump directly into the small intestine through a surgically placed tube. This ensures a flow of L-dopa that can be adjusted according to the patient's individual needs.

At least 12 cases of polyneuropathy related to vitamin B12 deficiency, and a case of Guillain-Barré syndrome have been reported in people with Parkinson's Disease treated with duodenal L-dopa infusion. L-dopa gel infusion may cause a decrease in vitamin B12 levels, leading to peripheral neuropathy. Other detrimental effects include alterations related to the metabolism of L-dopa, abnormal L-dopa absorption, and direct neurotoxicity of L-dopa at high doses. Vitamin B12 supplements may need to be considered in people with Parkinson's Disease on duodenal L-dopa infusion therapy, because vitamin B12 deficiency in people on duodenal L-dopa infusion therapy may be more frequent than the published data suggest.

In another new study, over a third (37%) of people with Parkinson's Disease were found to have neuropathy. Vitamin B12 deficiency was the most common cause. This could be made more likely by the long term use of L-dopa in any form. Many people with Parkinson's Disease who have neuropathy or Vitamin B12 deficiency are unaware of it.

Monday, January 30, 2012

DEMENTIA IS LINKED TO INSULIN RESISTANCE IN PARKINSON'S DISEASE

24th January 2012 - New research

Journal of Neurological Science [2012] Jan 20. [Epub ahead of print] (Bosco D, Plastino M, Cristiano D, Colica C, Ermio C, De Bartolo M, Mungari P, Fonte G, Consoli D, Consoli A, Fava A.) Dementia has been found to be associated with insulin resistance in Parkinson's Disease. Dementia commonly occurs in Parkinson's Disease when Parkinson's Disease progresses. This is not inevitable because the biochemistry of Parkinson's Disease and Dementia are completely distinct. There is therefore no reason why they should coincide. Their common association has never been fully explained apart from the fact that Dementia and Parkinson's Disease are both far more common with age.

People who have Parkinson's Disease and dementia were assessed for their resistance to insulin. When insulin is produced in order to prevent high blood glucose levels, insulin sometimes does not have affect. This can be due to insulin resistance, which is the inability of insulin to stimulate the insulin receptors. Brain function largely requires glucose in order to function. Nearly two thirds (62%) of people with Parkinson's Disease who had dementia were found to have insulin resistance. 30% of them also had impaired glucose tolerance. These percentages were significantly higher when the disease duration was longer and when the movement disability was worse. So dementia in Parkinson's Disease appears to be affected by the inability to make use of glucose rather than be a direct result of Parkinson's Disease.

THE PREVALENCE OF PAIN IN PARKINSON'S DISEASE

14th January   2012 - New research

Movement Disorders [2012] Jan 9 [Epub ahead of print] (M.P.Broen, M.M.Braaksma, J.Patijn, W.E.Weber)

Pain has been found to occur in over two thirds of people with Parkinson's Disease. Pain has been studied more intensely as a symptom of Parkinson's Disease in recent years. However, studies on the characteristics and prevalence of pain in Parkinson's Disease have given conflicting results, prompting a systematic review of the medical literature. In the relevant studies, the frequency of pain in Parkinson's Disease ranged from 40% to 85% with an average of 67% (just over two thirds of people). Pain in Parkinson's Disease is most frequently located in the legs, with almost a half (46%) of all people with Parkinson's Disease complaining about musculoskeletal pain. The pain fluctuates with on-off periods. A lot of the pain suffered is unrelated to the biochemistry of Parkinson's Disease, and is therefore not due to it. Surprisingly, only just over half (52%) of people with Parkinson's Disease with pain used analgesics (pain killers), most often non-opioids. This means that a lot people with Parkinson's Disease who suffer pain are going without any treatment for it.

MSU Researchers Identify Path To Treat Parkinson's Disease

Monday, January 30, 2012

MSU researchers have demonstrated the possibility of treating Parkinson's disease at its inception by treating the protein that triggers it before the disease can sicken the patient.

A team of researchers led by Basir Ahmad, a postdoctoral researcher at Michigan State University, has shown that slow-wriggling alpha-synuclein proteins are the cause of aggregation, or clumping together, which is the first step of Parkinson's.

The results are published in the current issue of the Proceedings of the National Academy of Sciences.

While scientists understand how proteins are structured, they do not yet know how they are built, a process known as folding. When errors happen infolding, proteins clump together, form plaques such as those found in Parkinson's disease, Alzheimer's and Lou Gehrig's disease, and cause cells to degenerate.

Lisa Lapidus, MSU associate professor of physics and astronomy and co-author of the paper, has dedicated her lab to researching folding.

"There are many, many steps that take place in aggregation, but we've identified the first step," she said. "Finding a method to fight the disease at its first stage, rather than somewhere further down the road,can hopefully increase the success rate in which the disease is treated."

The identification of this critical first step already has the researchers pursuing new ways to attack the disease. Lapidus is currently testing a number of naturally occurring compounds, which could push the rearranging protein out of the danger zone.

"We are now looking for molecules that can alter the protein when it first begins to ‘misfold,' which could eventually lead to the development of a drug that could prevent aggregation before it happens," she said. Yujie Chen, MSU graduate student, was one of the co-authors of the paper.

Source:http://www.wlns.com/story/16536510/msu-researchers-identify-path-to-treat-parkinsons-disease-at-its-inception

Saturday, January 7, 2012

URINARY DYSFUNCTION IN PARKINSON'S DISEASE

7th January 2012 - New research


Journal of Neurological and Neurosurgical Psychiatry [2011] 82 (12) : 1382-1386 (T.Uchiyama, R.Sakakibara, T.Yamamoto, T.Ito, C.Yamaguchi, Y.Awa, M.Yanagisawa, Y.Higuchi, Y.Sato, T.Ichikawa, T.Yamanishi, T.Hattori, S.Kuwabara)

Urinary dysfunction is common in Parkinson's Disease, but little is known about urinary dysfunction in early and untreated Parkinson's Disease. Nearly two thirds (64%) of people with Parkinson's Disease complain of urinary symptoms. However, there were found to be actual urinary problems in 85% of people with Parkinson's Disease. All of the 64% of people complaining of urinary symptoms had difficulty controlling the retention of urine, or lost control of urinary retention (storage abnormalities). Over a quarter (28%) had difficulty in urinating (voiding difficulties). Over half (58%) had detrusor overactivity. The detrusor muscle is the muscle that contracts when urinating to squeeze out urine. However, whilst urinating, detrusor underactivity rather than overactivity occurred in half of people.

These urinary symptoms were not correlated with gender, severity of Parkinson's Disease, or the type of motor symptom. Urinary dysfunction, manifested primarily as storage abnormalities, and with subclinical voiding difficulties commonly occurs in early and untreated Parkinson's Disease.

Friday, January 6, 2012

New Genetic Mutation Linked to Parkinson's

Using a new, cutting-edge technology for gene sequencing, researchers funded in part by the Parkinson’s Disease Foundation (PDF), have discovered a new gene called vesicular sorting protein complex 35 (VPS35) that is linked to Parkinson’s disease (PD) in people with familial PD. The results appear in the July 14 issue of the American Journal of Human Genetics.
In recent years, researchers have identified about a dozen genes that either cause PD or increase the risk of developing the disease. In general, the motor symptoms of PD begin at a young age in people who have mutations in genes that cause PD. People with mutations in the newly discovered gene, however, were diagnosed with PD around the age of 50.
To search for a new PD gene, an international team of researchers led by Carles Vilariño-Güell, Ph.D., and Matthew J. Farrer, Ph.D., at the University of British Columbia, Vancouver, focused on a family from Switzerland in which 11 people in three generations were diagnosed with PD. They compared the DNA of family members with PD to that of unaffected family members to search for differences that could explain why some developed PD and others did not.
In the past, this type of DNA analysis has been very difficult, requiring examination and DNA collection from large numbers of affected families. The University of British Columbia researchers instead used a new and efficient technique called whole exome sequencing, which focuses on small, but important, sentence-like sections of DNA. These sections govern the production of proteins. Since mutated proteins are most often the cause of genetic diseases, they reasoned that mutations linked to inherited PD would be found here.

Results

  • In all 11 members of the Swiss family who had PD, the scientists identified a mutation in the VPS35 gene.
  • Among 190 additional families that had many cases of PD, the researchers found the same VPS35 mutation in eight members of three families from the United States, Tunisia, and Israel (Yemenite Jews).
  • The VPS35 mutation was found in one person with no family history of PD.
  • The researchers tested DNA samples from more than 3,000 healthy individuals from several countries and found no mutations in VPS35.

What Does it Mean?

Like most other genetic causes of PD, this newly identified genetic mutation is exceedingly rare, resulting in very few cases of PD. However, these rare mutations have helped scientists generate key insights into the disease and a broad understanding of why people may develop PD. This new study is the first to implicate VPS35 in PD. Consequently, these results will need to be replicated in other populations in order to confirm this finding and assess the frequency of this mutation.
Nevertheless, VPS35 is already known to play a role in disease. The gene plays a central role in a neuron’s protein recycling center as part of the so-called retromer system. Breakdowns in the retromer pathway have already been linked to neurodegenerative diseases such as Alzheimer’s and Charcot-Marie-Tooth, the latter is a disease of the peripheral motor and sensory nerves. Therefore, a better understanding of how a VPS35 mutation causes cellular processes to go awry may help scientists unravel the causes of PD and other neurodegenerative diseases.
Reference: Carles Vilariño-Güell, Christian Wider, Owen A. Ross, Justus C. Dachsel, Jennifer M. Kachergus, Sarah J. Lincoln, Alexandra I. Soto-Ortolaza, Stephanie A. Cobb, Greggory J. Wilhoite, Justin A. Bacon, Bahareh Behrouz, Heather L. Melrose, Emna Hentati, Andreas Puschmann, Daniel M. Evans, Elizabeth Conibear, Wyeth W. Wasserman, Jan O. Aasly, Pierre R. Burkhard, Ruth Djaldetti, Joseph Ghika, Faycal Hentati, Anna Krygowska-Wajs, Tim Lynch, Eldad Melamed, Alex Rajput, Ali H. Rajput, Alessandra Solida, Ruey-Meei Wu, Ryan J. Uitti, Zbigniew K. Wszolek, François Vingerhoets, Matthew J. Farrer. VPS35 Mutations in Parkinson Disease. The American Journal of Human Genetics - 15 July 2011 (Vol. 89, Issue 1, pp. 162-167). www.cell.com/AJHG/abstract/S0002-9297(11)00242-4
Source Date: Jul 15 2011

BOXING LEGEND DIAGNOSED WITH PARKINSON'S DISEASE

9th December 2011 - News report


The former world boxing champion, the Colombian Antonio Cervantes, has been diagnosed with Parkinson's Disease. After Muhammad Ali he is the most successful boxer ever to have Parkinson's Disease. Antonio Cervantes grew up in Colombia shining shoes and selling contraband cigarettes in order to survive. He became a professional boxer whilst still only 18. He became the World Light Welterweight champion in 1972. He held the world title twice, from 1972 to 1976 and 1977 to 1980. He successfully defended his world title 16 times, and had a total of 21 world championship contests. He retired from boxing in 1983 having had 106 contests. Doctors said that he had serious health problems, including difficulties in communicating and eating. He is 65 years old.

NEW INHALED VERSION OF L-DOPA

2nd December 2011 - News release



The Michael J. Fox Foundation has awarded a grant to Civitas Therapeutics for clinical trials of CVT-301, which is a new inhaled version of L-dopa. It is claimed that CVT-301 has the potential to produce rapid, consistent and durable relief from the motor fluctuations associated with Parkinson’s Disease. Civitas has conducted a range of preclinical studies demonstrating CVT-301’s ability to deliver more rapid and consistent systemic exposure of L-dopa compared to the oral administration of L-dopa. The efficacy of oral L-dopa is significantly compromised by delayed absorption and excessive variability in the circulating drug concentrations. It is anticipated that the inhaled version of L-dopa would be used alongside the use of oral L-dopa. 

CVT-301 uses the ARCUS inhalation technology, which delivers a reliable and consistent drug dose with a compact, breath actuated inhaler. It uses a proprietary dry powder and inhaler combination that is unique in its ability to deliver a large, precise dose independent of inspiratory flow rate from a simple, easy-to-use device suitable for convenient self-administration. The platform has successfully delivered more than one million doses to patients incorporating active agents ranging from small molecules to large proteins.

PRAMIPEXOLE (MIRAPEX) INCREASES THE RISK OF HEART FAILURE

7th December 2011 - New research



Pharmacological Research [2011] Nov 23 [Epub ahead of print] (Mokhles MM, Trifirò G, Dieleman JP, Haag MD, van Soest EM, Verhamme KM, Mazzaglia G, Herings R, de Luise C, Ross D, Brusselle G, Colao A, Haverkamp W, Schade R, van Camp G, Zanettini R, Sturkenboom MC.)  The use of pramipexole by people with Parkinson's Disease has been found to increase the risk of heart failure. Pramipexole is a dopamine agonist that is also known as Mirapex, Mirapexin, or Sifrol. For more information go to Mirapex. Pramipexole increased the risk of heart failure in people with Parkinson's Disease by 61%. In the first three months of therapy, the risk of using pramipexole was far greater, as it trebled the risk of heart failure. The risk also increased with age, as the risk of heart failure in those people with Parkinson's Disease over 80 years old taking pramipexole was also trebled. When other dopamine agonists were assessed the researchers found no risk of an increase in heart failure in people with Parkinson's Disease.

INFLUENZA TREBLES THE RISK OF PARKINSON SYMPTOMS


15th December 2011 - New research



Influenza and other respiratory viruses [2011] 5 (5) : 328-333 (S.Toovey, S.S.Jick, C.R.Meier)

Influenza has been found to treble the risk of Parkinson symptoms. Influenza has been associated with Encephalitis Lethargica, a medical disorder causing the symptoms of Parkinson's Disease following the 1918 influenza pandemic.

Recent influenza (influenza in the past month) was associated with a trebling of the likelihood of Parkinson symptoms. Influenza some time in the past year was associated with only a small increase in the likelihood of Parkinson symptoms. The number of previous attacks progressively increased the likelihood of Parkinson symptoms. However, influenza did not increase the likelihood of actual Parkinson's Disease. The relevance of this research may be that people could be wrongly diagnosed with Parkinson's Disease, when what they have actually had is influenza. Around 25% of people are wrongly diagnosed with Parkinson's Disease and do not actually have it.

WORLD'S BEST EVER SQUASH PLAYER DIAGNOSED WITH PARKINSON'S DISEASE

9th October 2011 - News release


Jansher Khan, who is arguably the world's best ever squash player has been diagnosed with Parkinson's Disease at the age of 42, following a series of tests. During his career, Jansher Khan won the World Open a record eight times, and the British Open six times. Jansher Khan officially announced his retirement from squash in 2001. He had won 99 professional titles and was ranked the World No.1 for over six years. Jansher Khan has been showing signs of a mystery illness since last year. His hands would start shaking suddenly. Sometimes he used to act strangely as he his mind went out of control.

WIRELESS SENSOR FOR MEASURING PARKINSON'S DISEASE TREMOR

13th October 2011 - New product

Kinesia HomeView device has been developed to assess Parkinson's Disease tremor. It has been approved for sale in the U.S.A. and several other countries. It combines wireless sensors and a touch-screen tablet to help patients and physicians assess whether medications or neurostimulation therapy are working properly. The patient takes home a motion sensor worn on the finger, plus a touch-screen tablet that includes videos explaining how to take Unified Parkinson’s Disease Rating Scale tests. The tablet gives reminders to take the test several times a day. It measures tremors and, with a built-in camera, records videos of patients whilst taking the test. Patients can keep a diary of their symptoms on the tablet. Via a Web portal, physicians get a report from the system showing the types of tremors and the time of day of each test. Users can also watch videos of the tremors.

AZILECT FAILS TO SLOW PARKINSON'S DISEASE PROGRESSION

19th October 2011 - News release

In It has been claimed by the FDA (the U.S. drug administrators) that Azilect fails to slow the progression of Parkinson's Disease. Azilect is the brand name of Rasagiline, which is an MAO-B inhibitor. MAO-B inhibitors increase dopamine levels by inhibiting Monoamine Oxidase B, which is an enzyme that metabolizes dopamine. Rasagiline is used either on its own or alongside other methods.

The manufacturer, TEVA, claimed that the 1 mg dose of rasagiline (in the ADAGIO clinical study) and the 2 mg dose of rasagiline (in the TEMPO clinical study) could demonstrate a disease modifying benefit in patients with early untreated idiopathic Parkinson’s disease. However, the FDA's analyses "do not support the claim for a disease modifying benefit associated with either dose of rasagiline based on the primary protocol specified analyses or when sensitivity / secondary analyses are applied to the study data sets." For more information go to the FDA report.

In fifteen previous studies Rasagiline caused a moderate reduction in symptoms. It caused a moderate reduction in "off" time in four of those studies. The treatment effect was still evident six weeks after drug discontinuation. One of those studies found Rasagiline to be more effective than Selegiline, which is another MAO-B inhibitor. However, these studies did not demonstrate any slowing of Parkinson's Disease progression. Rasagiline caused infrequent cardiovascular or psychiatric side effects.

PROSAVIN CLINICAL TRIAL RESULTS FOR PARKINSON'S DISEASE

18th December 2011 - News release



Oxford BioMedica, a gene therapy company, have announced updated clinical data from a Phase I/II clinical trial of ProSavin for the treatment of Parkinson’s Disease. ProSavin uses Oxford BioMedica's own LentiVector gene delivery technology to deliver the genes for three enzymes that they suggest are required for the formation of dopamine, the substance whose deficiency causes Parkinson's Disease. The product is administered locally to the relevant region of the brain in order to increase the brain's own capacity for the formation of dopamine. For more information go to ProSavin.

The degree of efficacy is quite moderate and declines after six months. The average improvement in Parkinson's Disease symptoms for all the dosages was about 27% after 3 months. This improved slightly to about 31% after 6 months. The improvements started to decline after that down to 29% after 1 year, and declined further down to only 23% after 2 years. Three dosages were assessed : 1x, 2x and 5x. The level of efficacy declined when the higher 5x dosage was used. More results are expected in 2012 for the 5x dose. An enhanced administration procedure that facilitates higher dosing was used with some patients, but failed to demonstrate any additional benefit.

The safety profile was described as being favourable with no serious adverse events, but details of the side effects were not provided. Oxford BioMedica have claimed that the method could potentially provide more than a 10-fold increase in dopamine formation. However, the moderate improvement in efficacy is entirely inconsistent with that suggestion. Although they have claimed that three genes and enzymes are required for dopamine formation, only two of them are actually needed. Stimulating gene and enzyme levels artificially as they are doing reduces a person's own formation of those genes and enzymes, which is probably why the results start to deteriorate after six months.