Considering the essential difference between the pharmacological spectrum of selegiline and rasagiline,5 the results of the present study demonstrated that the group treated with selegiline as initial MAO-BI stayed without DA for a longer period compared with the rasagiline group; the hazard to initiate DA was twice as high in the rasagiline group compared with the selegiline group. This finding applied to the 4 age categories, although with some difference in HR values.
(I’m not sure how to interpret this paper.) I recently posted about substantial evidence of Selegiline being Neuroprotective whereas Azilect is less likely to be.
(Quote)Another possible explanation for the longer period until DA implementation in the selegiline-treated group is its better symptomatic effect that could delay the need for dopaminergic treatment
"So, which appears to have a higher possibility of being Neuroprotective, Rasagiline / Azilect or Selegiline? Tough decision."Do you think so? The selegiline article didn't convince me it was neuro protective and it was written before Azilect was developed. We also know that just about every drug that has been used in PD goes through a stage when it is claimed to be neuro - protective or slows the disease (including Sinemet) and in time it is realised this is not so.
The group treated with selegiline as initial MAO-B stayed without DA for a longer period compared with the rasagiline group; Weren't they an older age group? If so isn't there a general reticence to begin dopamine agonists in older people.
Hikoi ,however, according to some long-time neurologists here in Italy , selegiline remains one of the best drugs in its class. if I remember correctly you have been on this drug for many years and have a very slow progression it seems to me. Question: Would you recommend it today over other drugs or not?
No I am not on it now. I am on azilect. The big difference I think is that Azilect is a 24hr drug but selegiline is best not taken after midday because it can interfere with sleep. (It metabolises to an amphetamine). Azilect was developed specifically for PD. Selegiline for PD happened by chance.
In your earlier thread Raphaekg gives you a link that gives you answers to your question.
This is the article
Monoamine Oxidase-B Inhibitors for the Treatment of Parkinson’s Disease: Past, Present, and Future
“2017). A recent meta-analysis of the available clinical data confirms the effectiveness of MAO-B inhibitors both in monotherapy and in combination with levodopa. According to its results, selegiline seems to be the most effective MAO-B inhibitor in the combination therapy (Binde et al. 2018).”
“In the Finnish study 54 untreated patients were randomized to 10 mg/day selegiline or placebo. The median time to initiation of levodopa treatment was found about 6 months longer (Myllyla et al. 1991) and the necessary dose of levodopa for the sufficient therapeutic effect was about half in the selegiline group (Myllyla et al. 1993). The levodopa dose-sparing effect was not only maintained, but further increased after the 5-year follow-up period. Selegiline treatment also reduced the need of additional dopaminergic therapy (slow release levodopa or dopamine agonist) (Myllyla et al. 1997). In a Swedish study of 157 early PD patients, selegiline significantly delayed the need to start levodopa therapy by about 4 months compared to placebo. Furthermore, the advantage of selegiline treatment in UPDRS scores was maintained after 2 months washout period before levodopa was started suggesting its neuroprotective effect (Palhagen et al. 1998). In the continuation of this study, the advantage of selegiline was also maintained after levodopa was started. Patients after 5 years on selegiline and levodopa combination had nearly ten points lower UPDRS scores, while 19% lower levodopa dose was used compared to levodopa only group (Palhagen et al. 2006). Recently, the benefit of selegiline monotherapy in early PD was also confirmed in a 12-week controlled trial in Japan, further supporting the use of the drug in early Parkinsonism (Mizuno et al. 2017).”
MAO-A inhibitors increase dopamine levels. MAO-B inhibitors do not. ?! This is surprising!
“MAO-A inhibition by clorgiline significantly increased the levels of phasic and basal DA, which could be attributed to a blockade of DA metabolism. Moreover, ex vivo whole-cell patch-clamp experiments revealed that MAO-B plays an important role in astrocytic GABA-mediated tonic inhibition, whereas MAO-A does not. Taken together, our findings provide conclusive in vivo evidence for resolving the controversy on the role of MAO-B in DA metabolism, which has continued over several decades. (Fig. 5).”
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Help in understanding drugs in Parkinsons
