• N&PD Moderators: Skorpio

substances that stimulate brain cell growth

Good morning yall,


ive got a few questions regarding regarding substances and neurogenisis

First off, whats the final word on alcohol and neurogenisis does it decrease it or increase it as its a NDMA antagonist (ive read that NDMA antagonists such as ketamine increase BDNF or something)?

Grue mentioned that citicholine stimulates neurogenisis, would choline bitartrate do this too?

Does piracetam do anything for neurogenisis?


omega-3 fatty acids

Is this true?
 
Piracetam possibly, but it could be through indirect action such as the subject being more willing to engage in obtainment of new information (ie, studying & learning and gaining more neural connections) so hard to say without very detailed testing (possibly not all available anyways). By this logic, adderall could provide false positives as well. =P

Anyways I think the issue for now is less about brain cell "growth" than brain cell "health" and "function." A healthy brain capable of proper function will "grow" properly (that is, make perfect, new functional synaptic connections with 100% efficiency). Many of the substances listed in this thread & forum will help with that.

And in all honesty, despite the strong evidence for hippocampal neurogenesis across species, no one really knows (as far as I am aware) what it truly functions to do or at what rate it occurs in humans.
 
The following are either antiapoptotic, synaptogenetic, neuroprotective (either directly or allosterically), upregulate endogenous neurotrophic factors, or directly stimulate the production of new neurons from stem cells. (and I'm sure they produce other effects, as well)

nerve growth factor
brain-derived neurotrophic factor
neurotrophin 1/2/3/4
dihydrotestosterone
testosterone
aromatase
pregnenolone sulfate
long-term administration of NSAIDs
curcumin (also conduces to apoptosis in cancerous cells)
galanthamine
protein kinase M zeta
cyclic adenosine monophosphate responsive element binding protein (CREB)
cypin & tubulin
T-588
l-acetylcarnitine
l-creatine
l-theanine
fluoxetine (and probably other SSRIs)
sodium valproate
AIT-082/Neotrofin
almitrine-raubasine
phosphatidylserine
phosphatidylcholine
docosahexaenoic acid (DHA)
docosahexaenoic acid + cytidine diphosphate choline (citicoline) + uridine 5' monophosphate (UMP)
cytidine diphosphate choline (alone)
carbenoxolone
nimodipine (NIM)
cerebrolysin
hyperforin
Idebenone
dimebolin hydrochloride
growth-associated protein 43 (GAP-43)
ghrelin
GVS-111 / Noopept / DVD-111
rolipram and other phosphodiesterase 4 inhibitors
selegiline
rasagiline
hydergine
desferal
VK-28
moclobemide
vinpocetine
MW01-5-188WH
exercise
caloric restriction (Perhaps because of the high levels of ghrelin and low levels of cholecystokinin associated with caloric restriction?)
 
Inducing cell proliferation in the CNS sounds like a super duper way to give yourself any of many different CNS cancers.

Concussions and spinal cord damage will also cause your brain to begin things like astrocytosis and gliocytosis.
 
Abstract of WO 2008001369 (A1)

The present invention relates to ligands of the peripheral cannabinoid receptor CB2, especially (+)-a-pinene derivatives, and to pharmaceutical compositions thereof, which are useful for promoting, inducing and enhancing neurogenesis including neural cell regeneration. In particular, pharmaceutical compositions of the invention will be useful for preventing, alleviating or treating neurological injuries or damages to the CNS or the PNS associated with physical injury, ischemia, neurodegenerative disorders, certain medical procedures or medications, tumors, infections, metabolic or nutritional disorders, cognition or mood disorders, and various medical conditions associated with neural damage or destruction.

http://v3.espacenet.com/publication...008001369A1&DB=EPODOC&locale=en_EP&CC=WO&FT=D
 
apparently stress & depression decreases the ammount of brain cell growth (if i read the abstract right lol):

Background: One of the most consistent morphologic findings in postmortem studies of brain tissue from depressed patients is a decrease in the number of glia in the prefrontal cortex. However, little is known about the mechanisms that contribute to this decrease in cell number.
Methods:To address this question, we subjected adult rats to chronic stress, a vulnerability factor for depression, and measured cell proliferation as a potential cellular mechanism that could underlie glial reduction in depression.
Results: We found that exposure to chronic unpredictable stress (CUS) for 15 days significantly decreased cell proliferation in neocortex by approximately 35%. This effect was dependent on the duration, intensity and type of stress, and was region-specific. Analysis of cell phenotype demonstrated that there was a decrease in the number of oligodendrocytes and endothelial cells. Finally, using a CUS paradigm that allows for analysis of anhedonia, we found that chronic antidepressant administration reversed the decrease in cortical cell proliferation, as well as the deficit in sucrose preference.
Conclusion: These findings are consistent with the possibility that decreased cell proliferation could contribute to reductions in glia in prefrontal cortex of depressed subjects and further elucidate the cellular actions of stress and antidepressants. [source]
 
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