From bdb7d7939c30bb2cbaf900ac66a0ec39d753c314 Mon Sep 17 00:00:00 2001 From: Freeman O'Hea Date: Wed, 14 Oct 2026 16:29:09 +0800 Subject: [PATCH] Add Rasagiline : a Neuroprotective Smart Drug ? --- Rasagiline-%3A-a-Neuroprotective-Smart-Drug-%3F.md | 9 +++++++++ 1 file changed, 9 insertions(+) create mode 100644 Rasagiline-%3A-a-Neuroprotective-Smart-Drug-%3F.md diff --git a/Rasagiline-%3A-a-Neuroprotective-Smart-Drug-%3F.md b/Rasagiline-%3A-a-Neuroprotective-Smart-Drug-%3F.md new file mode 100644 index 0000000..1bcbdb0 --- /dev/null +++ b/Rasagiline-%3A-a-Neuroprotective-Smart-Drug-%3F.md @@ -0,0 +1,9 @@ +
Rasagiline is typically well tolerated if used within the therapeutic dosage range. In one study, the efficacy of 1 mg rasagiline taken once daily was similar to 200 mg of the COMT inhibitor entacapone (Comtan) administered with each levodopa dose: the only adverse event reported to be significantly more common with rasagiline than with the placebo was postural hypotension. Most recently, the well-controlled PRESTO study of the Parkinson Study Group confirmed an improvement in motor fluctuations and Parkinson's disease symptoms in levodopa-treated patients; the only adverse events significantly more common with rasagiline than with the placebo were reportedly balance difficulties in the 0.5 mg rasagiline group, and anorexia, vomiting and weight loss in the 1 mg group. Fewer patients reported depressive symptoms. In the LARGO study, the frequency of adverse side-effects in patients using rasagiline or entacapone as adjuncts to levodopa treatment was similar to those in patients taking the placebo.
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At dosages above around 2 mg per day, rasagiline loses its selectivity for MAO type B and also inhibits MAO type A. An MAO-B selective regimen does not cause significant tyramine potentiation, the dreaded "cheese effect" common to users of older unselective and irreversible MAOIs who eat tyramine-rich foods. Thus low-dosage rasagiline demands no special dietary restrictions. But rasagiline should not be combined with other MAO inhibitors, [The Genius Switch Official Website](https://maxmeta.io/index.php/FORCE_FACTOR_Forebrain_Nootropic_Brain_Supplement_Review) selective or otherwise. Concomitant use of the opioid painkiller pethidine (meperidine, Demerol) is contraindicated too. For poorly understood reasons, combining SSRIs with rasagiline is also best avoided even at a low MAO-B selective dose. The optimal dosage of rasagiline has yet to be exactly established, whether for Parkinsonians, or for depressives who may benefit from higher rasagiline dosages that inhibit both types of MAO enzyme, or for use of rasagiline prophylactically as a neuroprotectant by the "worried well", i.e. sufferers from the fatal hereditary disorder we know as the ageing process.
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Over the clinical dosage range, rasagiline displays a more-or-less linear pharmacokinetics. An excessively high dosage of rasagiline apparently shrinks [The Genius Switch Official Website](https://wikivora.org/wiki/User:MarcJarrell865) cell sizes of nigral tyrosine hydroxylase-positive neurons. This is currently of unknown significance, but suggests a dose-effect graph with an [inverted U](https://www.groundreport.com/?s=inverted%20U) shape, possible toxicity, and consequently the need for caution. The effects of a long-term regimen of rasagiline on human life-expectancy and maximum lifespan are unknown. Yet since low-dosage selegiline can increase both life-expectancy and maximum lifespan in a number of non-human animal species, it is possible, though again unproven, that rasagiline's superior metabolic profile may offer advantages for life-extension. The only other current routes to enhanced longevity are either caloric restriction (CR) - which takes brutal self-discipline and can compromise mood, virility and vitality - or, hypothetically, the use of compounds like resveratrol which mimic the effects of caloric restriction without provoking its troublesome side-effects. But they remain clinically unproven too.
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Rasagiline doesn't displace catecholamines from their intracellular stores. It lacks any significant "abuse potential", though this is seldom a problem with selegiline either. Neither acute nor chronic rasagiline taken at MAO-B selective dosages increase tissue levels of [The Genius Switch focus program](http://racist.wiki/index.php/User:GeraldHamlin9) monoamine neurotransmitters noradrenaline, serotonin and dopamine. In common with selegiline, rasagiline may be protective against the serotonergic damage caused by the widely used drug MDMA (Ecstasy). Unfortunately, the risks of taking any MAOI with MDMA probably statistically outweigh any neuroprotective benefit. A post-E fluoxetine (Prozac) or other SSRI may offer a less hazardous form of neuroprotection; but this carries theoretical risks too. Until safe and sustainable insight-and-empathy drugs are developed, it may be prudent either to use them only very sparingly or avoid them altogether. An enriched conception of mental health is of limited use until we have [The Genius Switch binaural beats](https://freakapedia.com/index.php/The_Genius_Switch_Reviews:_Unlocking_Your_Mind%E2%80%99s_Potential) means to sustain it. If rasagiline is good news, then other pharmaceutical products on the commercial horizon are better.
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Perhaps most notable is the neuroprotectant ladostigil (TV3326), again designed by the redoubtable Professor Youdim. Ladostigil inhibits both cholinesterase and MAO activity, enhancing cognitive function and mood alike. Ladostigil is cunningly designed with a propargyl group for MAO inhibition and a carbamate moiety to inhibit cholinesterase. Both the MAO type A and MAO type B inhibition of ladostigil are relatively selective to the brain: liver and small intestine enzymes are less affected. This advance is important for several reasons. One reason is obviously the plight of a rapidly growing population of [elderly Parkinsonian](https://www.wonderhowto.com/search/elderly%20Parkinsonian/) and Alzheimer's patients in need of more effective drug therapies with fewer risks and adverse side-effects. But the potential range of therapeutic application is broader. Most people would like to feel happier, smarter, younger and sexier. Sadly, contemporary antidepressants and nootropics are badly flawed. It's not just that they are often ineffective. They either have anticholinergic "dumb drug" effects like the older tricyclics, or they flatten emotions and kill libido, like the SSRIs. Older unselective, irreversible MAOIs like tranylcypromine (Parnate) and phenelzine (Nardil) can elevate mood, but their risks and accompanying dietary restrictions make them unattractive even for the clinically depressed and their wary physicians. Meanwhile classic nootropic agents such as cholinergic boosters are liable to subdue mood and cause behavioural inhibition. The attraction of dual action agents like ladostigil, on the other hand, is that they promise to lift mood and intellectual performance alike, while offering a measure of protection against the ravages of ageing. Even so, tomorrow's neuroprotective smart mood-brighteners are just stopgaps. They offer only palliative relief on the route to germ-line gene therapy in decades to come, and perhaps the wholesale genomic rewrites of the posthuman era beyond. The global pandemic of human ageing can ultimately be cured; but eradicating the lethal disorder we call old age may still take several centuries.
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