Teva says Azilect slows progression of Parkinson's
 

The info is little .. the drug is expensive ..I understand it interferes with supplements .. I have my doubts ..
what do you think?

http://money.cnn.com/news/newsfeeds/...c2c2b9cee0.htm
NEW YORK (Associated Press) - Teva Pharmaceutical Industries Ltd. on Monday said trial data from its Parkinson's disease drug Azilect showed it can slow the progression of the disease.

Parkinson's drugs, including Azilect, are approved to treat symptoms of the disease.

The trial, which enrolled 1,176 patients with an early stage form of Parkinson's, met its goal in three areas, including a change in a common measurement used to assess disease status.

well, I think......
 

that if you believe that, I have some beach front property in Arizona thats for sale!!

Seriously, I think it is damn near impossible to quantitfy this assertion. I think that it is an oft repeated sales ploy that in time will be debunked. Hope I am wrong, but I don't think so......

Charlie

I have $1,000.00 worth of it in my kitchen. Took one pill and had such bad dyskenisa I couldn't even stay on the bed. Learned the lesson to ask for a sample before filimg a prescription. Expensive lesson.

Didnt they say the same thing about Mirapex? :D

Yeah, I think the more generalized recent conclusion is that the agonists hasten the disease process. Azilect is an MAO inhibitor of some kind. As is mucuna. I cast my vote with mucuna. It`s cheaper and works pretty good.

In their time I think ...
 

most drugs associated with the "PD space" have made this claim. Its the law of pharma marketing.

I even remember having the same claims being made for DBS and L-dopa.

Antioxidents, nicotine, caffeine, meeting the previous Pope, etc, all have claimed to delay PD, (or cure it in the case of the Pope). I tend to rely on the advice of forum members like Ron and Everitt.

Take care,
Neil.

This is a milestone
 

I believe this is the first drug that has actually shown verifiable disease modification in clinical trials. TEVA's "Adagio" trial was a year and a half long trial in 14 countries, based on protocol design suggestions from the FDA.

If the FDA approves this application, this is the first approved disease modifying drug for PD, which in and of itself is a big event.

Maybe some have had adverse reactions to it, but this is still a major milestone and something to be cheered.

Just my humble opinion.

Oh, and hello everyone. :)

(MB Youdim, MD, one of the principal developers of Azilect, maintained inhibiting just MAO-B doesnot stop the breakdown of dopamine; that MAO-A is also necessarry in conjunction with MAO-B for that to occur. He stated at the WPC in 2006 that azilect works by regulating the apoptotic pathway in the mitochondria and also prevented opening of the permeability transport pores of the mitochondrial membrane. the following is from 2003, when the data did not support neuroprotection from azilect...we are hopeful it is neuroprotective since my husband takes 1mgm/day.

http://www.rasagiline.com/propargylamines.html

Anti-apoptotic function of propargylamine
inhibitors of type-B monoamine oxidase
by
Naoi M, Maruyama W, Youdim MB, Yu P, Boulton AA.
Department of Brain Sciences,
Institute of Applied Biochemistry,
Yagi Memorial Park, Mitake, Kani-gun,
Gifu 505-0116, Japan.
Inflammopharmacology. 2003;11(2):175-81.

ABSTRACT
In Parkinson's disease and other neurodegenerative diseases, (_)deprenyl, an inhibitor of type B monoamine oxidase (MAO-B), has been proposed to protect or rescue declining neurons. However, clinical trials failed to confirm the neuroprotection, even though in vivo and in vitro studies suggested the possibilities. This paper describes the activities of propargylamine MAO-B inhibitors against apoptosis induced by an endogenous selective dopaminergic neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells. A series of propargylamines were shown to suppress the apoptotic cascade; preventing collapse of mitochondrial membrane potential, activation of caspase 3 and fragmentation of nucleosomal DNA. Among propargylamines, (R)-N-propargyl-1-aminoindan (rasagiline) was the most potent at preventing cell death. Rasagiline also prevented opening of permeability transition pore in insolated mitochondria. These results suggest that rasagiline and other propargylamines may regulate the apoptotic machinery in mitochondria and rescue or protect deteriorated neurons in neurodegenerative disorders.

Madelyn, I've read about the developer of Azilect, MB Youdim, and I have faith in him, so I don't think of big pharma when I think of Azilect.

He also thinks green tea is protective.


http://www.sciencedirect.com/science...2499b1f8c897b2

http://journals.elsevierhealth.com/p.../MDLN.16470637

http://nootropics.com/smartdrugs/future.html

AN OLD ARTICLE:


Personal quest inspires research
BARRY COHEN

Professor Moussa Youdim is working for personal reasons to discover the secrets underlying the causes and treatments for neuro-chemical disorders such as Parkinson's and Alzheimer's diseases.

In 1957, his father had a depressive illness and had to travel from Iran to England to receive treatments. Doctors only knew to treat him with shock treatments, recalls Youdim.

"I saw my father's personality change," he says. "He recovered, but he was not the same person again."

"There were no neuro-psychiatric drugs at that time," he adds, referring to the 1950s and early 1960s.

After witnessing his father's struggle and its aftermath, Youdim decided to change his focus at McGill University in Montreal from pre-medicine to biochemistry and neurochemistry.

"I thought the great frontier was understanding how the brain works," he says.

Youdim spoke about his efforts to treat and cure Parkinson's and Alzheimer's diseases Feb. 9 during a luncheon at the Phoenix Country Club. Youdim is the Finkelstein Professor of Life Sciences in the faculty of medicine at the Technion (Israel Institute of Technology) in Haifa, Israel.

Youdim took a roundabout way to Israel.

He was born in Iran but his parents, in order to provide for his education, sent him to a boarding school in England. Youdim says he accepted the "European lifestyle" and never moved back.

He continued his education in Montreal, where he earned a Ph.D. in biochemistry from McGill University. He then returned to England to continue his research.

Officials from Technion University in 1977 invited him to set up a department of pharmacology. He accepted the offer and made aliyah in 1979, becoming an Israeli citizen.

"I thought it might be a good idea. It was challenging," said Youdim. "It was nice to create something from scratch."

Youdim and his ex-wife Elizabeth have 20- and 22-year-old sons and a 15-year-old daughter.

The Technion, which opened its doors in 1924, is Israel's oldest and premier institute of science and technology. Its first undergraduate class had 16 students. Less than 70 years later, boosted by immigration from the former Soviet Union, the student body increased to 10,500.

Technion's Web site explains that the curriculum now includes the latest in high-tech research, nuclear power, marine engineering and industrial robots. The majority of Israeli-educated scientists and engineers received degrees from Technion.

The university has led to the high-tech boom in Israel, says Youdim. The nation now has its own version of California's Silicon Valley.

In addition, a "symbiotic relationship" exists at Technion because the engineering school is connected with the medical school through interdisciplinary studies. This will ensure Technion is on the forefront of "21st-century medicine and the development of hi-tech and biotechnology and pharmaceuticals," he says.

One example is the inroads Youdim has made at Technion with the drug Selegiline. Developed in Hungary, the medication is a failed anti-depressant, says Youdim. However, he helped discover that it is an effective treatment for symptoms of Parkinson's such as muscular rigidity; tremors; bradykinesia, slowness of movement; and poor balance, characterized by sudden falls.

"The jury is out as to whether (Selegiline) has neuro-protective qualities," says Youdim, which would prevent the progression of Parkinson's disease.

"Nerves communicate with each other through chemical means," says Valley neurologist Dr. Barry Hendin. Separated by gaps, or synapses, nerve cells use chemicals called neurotransmitters to activate or inhibit messages shared between them.

The neurotransmitter related to Parkinson's is dopamine.

"If you lose the neurons which store and release dopamine, you lose fluidity of movement," says Hendin.

When cells that store the neurotransmitter acetyl-choline die, "there is too little of the transmitter that allows effective intellectual processing," he explains, such as memory, cognition and language proficiency. The result is the onset of Alzheimer's.

Youdim is now developing a new drug, Rasagaline, to treat Alzheimer's disease. It is currently in "Phase III," when the drug is first tested in people to determine its effectiveness and side effects. At this stage, data is collected to receive Food and Drug Administration approval.

In Phase I, scientists determine the pharmaceutical properties of a new drug; In Phase II, the drug's safety is tested in the lab; Phase IV occurs after FDA approval, when developers test the results of changing drug dosages or its vector - administered tablet or liquid form, or injected.

Youdin says one of his goals at Technion is to "develop drugs to prevent the progression of (Parkinson's and Alzheimer's) and prevent the process of neuro-degeneration," the steady deterioration of neurons leading to cell death.

A long-term goal is to develop "neuro-rescue" treatments to reverse the damage done by the diseases, he adds.

Harold Morgan, former executive director of the Jewish Federation of Greater Phoenix, is a consultant to the American Technion Society, which supports and promotes Technion's research achievements. He sees Youdin's visit as a means to strengthen the connection between Jews in the Diaspora and Israel.

Technion's development of treatments for Parkinson's and Alzheimer's change the way Diaspora Jews view Israel, says Morgan....

http://www.jewishaz.com/jewishnews/010302/quest.shtml

Maybe......
 

We will eventually see if it pans out.

A couple of years ago I thought rasageline was going to be a truly effective blockbuster, but so far I'm not convinced. For the time being my money is on low-dose naltrexone or dextromethorphan with high-dose CoQ10, along with the minimum effective dose of l-dopa/carbidopa and amantadine.