It's often said that all of the treatments currently in use for Parkinson's offer symptomatic relief only, and do not affect underlying pathology. However, a recent study suggests selegeline use impacts white matter microstructure and could be neuroprotective. I know white matter abnormalities have been found in REM Behavior Disorder, which makes me wonder if selegeline use in this prodromal stage could help stave off some symptoms. The areas most affected by selegeline seem to involve depression and cognitive function, both known to be associated with RBD.
Glad to hear that, Park Bear. Is it a well-tolerated med?
Seems like RBD would be the perfect circumstance to trial a known medication with proven neuroprotective attributes, especially in those prone to depression. I wonder if enough money could ever be raised to do a study like that though. I don't imagine there's much profit to be had in repurposing an older, presumably generic drug.
As far as I know it is well tolerated. I've been taking it for years and I've not experienced any adverse effects personally. nor do I recall complaints from others here.
It is generic and I agree not likely to get much funding for a trial.
I don’t know any of the technical medical reasons for prescribing selegeline. Only that it was the first medication that my doctor prescribed a year after my PD diagnosis 6 yrs ago. Selegeline (5mg) was the sole prescribed med that I took for 3 years. About one and a half yrs ago my doc added C/L extended release (25/100mg ) 4x a day. I continue to take the selegeline. I try to fast walk an hour a day as well and am doing well.
Ît was the first med that I took aswell. My doctor took me off it because it didn't seem to be doing anything. Plus I seen to remember that it was discredited in some study as being ineffective? But isn t it the most commonly prescribed med for pd in England? What are the results there?
"But isn t it the most commonly prescribed med for pd in England? What are the results there?"
I don't know, hopefully someone from the UK will weigh in.
One problem I see is that using a medication for motor symptom relief (what I think most docs are trying to achieve?) could be different from using it for neuroprotection, where I "think" the goal would be to slow disease progression.
"Selegiline is metabolised into L-(−)-desmethylselegiline (DES), L-(−)-amphetamine (A) and L-(−)-methamphetamine (MA), mainly in the liver."
"Due to the stereospecificity and the low CSF concentrations of the (−)amphetamine metabolites during the therapy with 10 mg selegiline, these metabolites do not seem to contribute significantly to the clinical efficacy of selegiline."
So it appears that the metabolites you mention are present in low amounts and don't actually "do anything." On the other hand, the third metabolite they mention, but that you did not (desmethylselegiline) may be neuroprotective;
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