Quote (shane_is_a_balla @ Dec 8 2016 03:52pm)
Not surprising, this is a known effect of MAOIs. The issue is their abundance of side effects, however, especially things like vomiting, egregious nausea, and so on. It has implications for depression and various co-morbidities because they're thought to cause gradual hippocampal atrophy, perpetuating depression/loss of emotional control, elevating glucocorticoids for other deleterious effects, and promoting cognitive decline & memory decay. But again, we know this to be the case from MAOIs, we just can't administer them due to adverse effects. Perhaps the specific molecule (DYRK1A) can be a novel target to bypass the effects of raising monoamine transmitter concentration, though, and still achieve neurogenesis.
As for a fixed number of divisions, etc, that's nonsense. Neurogenesis occurs throughout our lifetimes, albeit at a gradually slower pace. Further, it would have zero implications for normal replacement of deceased neurons in other areas of the brain, sans those few areas that we know encompass our few neurogenic niches (subgranular zone to DG of hippocampus, and subventricular zone to olfactory bulb, as well to the striatum). If we're talking about replacing neuronal death, such as with Parkinson's disease to exemplify the issue, we would need to either learn to induce neurogenesis, and then also specific migration and induction into that sub-tissue, or learn to manipulate stem cells to differentiate how we please (we have) and inject them specifically. Certainly, both avenues have merit, but there's far more progress done heretofore in the latter, and it also seems far more plausible due to specificity, etc. That would of course by extension be applicable to other areas, such as cortical ones with strokes, etc. Now, coming back to the issue of inducing neurogenesis to happen with greater celerity and w/ more magnitude, I think it's certainly debatable how appreciable the atrophy of brain tissues under depression, chronic stress, etc, really is. What I mean is - differentiating between neurogenesis and synaptogenesis/synaptic contact. There seems to be more evidence that it's more-so dendritic retraction (as opposed to arborization), and pruning of synapses in general, than it is specific death of neurons or loss of neurogenesis. For a quick example of how robust this can be (as it may not be intuitive), what appears to antecede schizophrenia is a massive pruning of the cortex, enough to be measured as an actual thinning - all purely from loss of synaptic contact. This ofc occurs as a teen, in a measurable way, but the process seems to get carried away in those afflicted, hence symptoms beginning late adolescence/early adulthood. Back to the point, I just didn't want too much emphasis on inducing neurogenesis to be placed, albeit it still may be therapeutic. MAOIs, various antidepressants, ketamine (experimental antidepressant inducing its effects in an extremely short time-frame due to rapid increased AMPA conduction in the PFC, causing synaptogenesis), etc, all induce this effect in some way.
Dead neural tissue is dead tissue. If you destroy the soma, it's not coming back. You can damage or sever axons and they will regenerate but once the cell body is dead the neuron is dead. Unless by neurogenesis you are referring to the healing of axons. Why do you think stroke survivors have such permanent functional loss? The cortex is highly plastic and the remaining tissue will rearrange it's functional organization but once neurons die they are dead and not replaced