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Life Extension Magazine

LE Magazine September 1996

The Deprenyl Controversy

Recent papers in the British Medical Journal (BMJ) and Annals of Neurology (AN) have called into question the value of deprenyl as a treatment for Parkinson's disease. After a series of positive studies on deprenyl, starting in the mid 1980s, these papers have doctors around the world debating whether they should continue to prescribe deprenyl for Parkinson's disease.

Big Ben As one of the earliest advocates of deprenyl for Parkinson's disease, Alzheimer's disease and as a general anti-aging therapy, the Life Extension Foundation has analyzed the findings of these papers in the context of past findings on deprenyl, and has re-evaluated our recommendations of deprenyl.

The British Deprenyl Study

In the December 1995 BMJ, a paper by A.J. Lees (on behalf of the Parkinson's Disease Research Group of the United Kingdom) reported the findings of a multi-center (93 hospitals) open clinical trial.1 This trial compared standard L-Dopa treatment (including a dopa decarboxylase inhibitor) to the combination of L-Dopa and deprenyl in 520 early-stage Parkinson's patients after an average of 5-6 years of follow-up.

The Rationale Behind L-Dopa Treatment

The rationale behind the standard L-Dopa treatment, which has been in routine use for the past 25 years, is that L-Dopa, the precursor of the neurotransmitter dopamine, serves as a substitute source of dopamine, replacing dopamine lost after the death of dopamine-secreting neurons in the substantia nigra region of the brain.

The accelerated depletion of dopamine in the brain resulting from the destruction of these neurons is the primary cause of Parkinson's disease. Since dopamine plays an important role in movement, coordination, strength, sex drive, and cognitive function, Parkinson's patients suffer from progressive movement and cognitive disorders that greatly reduces the quality of their lives and shortens their lifespan.

A Short-Lived "Miracle"

When L-Dopa was first given to Parkinson's patients in the 1960s, it was widely hailed as a "miracle" drug because of the dramatic improvements in function it produced. But when longer-term studies were conducted, it was found that the benefits were short-lived, that the drug does not slow the progression of Parkinson's Disease, and that it produces serious adverse side effects, including involuntary movements, fluctuations in motor performance and mood, and psychiatric abnormalities.2 As a result, doctors began reserving L-Dopa for moderately or severely impaired patients, where its functional benefits outweigh its side effects.

The Dilemma For Parkinson's Doctors

For decades, doctors searched for a therapy that could help early-stage Parkinson's patients without adverse side effects. BrainTheir dilemma was that at diagnosis most Parkinson's patients have lost up to 80% of their dopaminergic neurons.3 By the time the symptoms of the disease begin to seriously interfere with the quality of their lives, they've already lost almost all of their dopamine-producing neurons. L-Dopa is merely a source of dopamine. It cannot prevent the ongoing loss of neurons, but only provides temporary symptomatic relief.

The Promise Of Deprenyl

That's why doctors were so excited when deprenyl (also known as selegiline), a drug developed by Joseph Knoll of the University Of Semmelweis in Hungary, came on the scene in the 1980s. A series of positive studies suggested that deprenyl might not only improve the quality of life for Parkinson's patients, but might also slow the progression of the disease.

These studies showed that deprenyl could extend lifespan in laboratory animals, 4 restore lost sex drive in animals,5 and neutralize the deleterious effects of powerful neurotoxins such as MPTP (l-methyl-4-phenyl-1,2,3,6-tetrihydropyridine)6 and 6-hydroxydopamine.7 Doctors were especially intrigued by deprenyl's ability to counteract the effects of MPTP, which produced severe Parkinsonian symptoms in young people who took it as a "street drug", and which induces a Parkinson-like syndrome in laboratory animals.