Posted by djmmm on March 24, 2005, at 11:09:44
In reply to Re: does Parnate or Selegine produce cell growth? » SLS, posted by Sarah T. on March 24, 2005, at 0:23:26
> > > > The article and the bibliography citations for the article were written prior to 1993. It has since been debated whether it is truly neuroprotective or not. I think much of the newer work refutes the neuroprotective effects of deprenyl.> - Scott
> >
>
> Hi Scott. A couple of years ago, my psychiatrist told me exactly what you just mentioned, i.e., that more recent research refutes the neuroprotective effects of deprenyl. Even before he said that, I found it difficult to believe that a drug that metabolizes into methamphetamine could be neuroprotective.
>
>MAO-B inhibition attenuates the oxidization of dopamine into nurotoxins (6-hydroxydopa and 6-hydroxydopamine)
The neuroprotective rationale behind MAOb inhibitors is twofold: firstly, referring back to Equation 1, if MAOb is inhibited, less H2O2 is produced and thus fewer OH• are produced which limits oxidative stress. In addition, Selegiline induces free radical scavenging enzymes, SuperOxidase Dismutase (SOD) and catalase which will limit free radical damage [18]. Secondly, MAOb is required for the conversion of MPTP to MPP+ [Figure 4] so if any such toxin (either endogenous or exogenous) is responsible for PD, limiting this reaction would have neuroprotective benefits. Indeed, increased longevity has been reported for selected selegiline patients [22]. Selegiline is metabolised to amphetamines and desmethylselegiline. The latter has been shown to reduce apoptotic neuronal death in vitro [19] . Higher ratios of this metabolite is achieved via the transdermal [20] or subcutaneous [19] routes which are now being explored for neuroprotective effects.http://www.chemsoc.org/exemplarchem/entries/2003/nottingham_russell/2.html
poster:djmmm
thread:474314
URL: http://www.dr-bob.org/babble/20050322/msgs/474941.html