Selegiline Induces “Trophic-Like” Rescue of Dying Neurons without MAO Inhibition
Selegiline has been claimed to slow the progression of motor deficits in Parkinson’s Disease (PD)1 and cognitive decline in Alzheimer’s Disease (AD).2 It is controversial whether the slowing represents a symptomatic action due to improved dopaminergic neurotransmission or neuroprotection due to a decrease in the production of toxic oxidative radicals consequent on the inhibition of monoamine oxidase B (MAO-B). We propose a third action for selegiline — a “trophic-like” rescue of dying neurons.
KeywordsGlial Fibrillary Acidic Protein Dopaminergic Neurotransmission Trophic Support Symptomatic Action Ticial Motor
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