Wanted to hear everyone's opinion on this theory: What if racetams are completely misunderstood, and their mechanism of effect is an antibiotic, antiprotozoal or antifungal effect on chronic infections of the CNS? This would explain why almost no effect is seen in young, healthy specimen - they don't have any infections to affect, and why many people develop tolerance - the infection develops a resistance to the racetam.
It might not be the racetam itself, but rather some metabolite of the racetam, that has the actual antibiotic/fungal effect.
Also entirely possible is that racetams have some minor nootropic effects, such as modulating AMPA receptors in the case of Aniracetam, increasing expression of BDNF (even though I would suspect this to be an indirect effect of destroying infected cells), etc. - and then one of the metabolites has an antibiotic or antifungal effect which does the heavy lifting in those who experience considerable benefit from racetam usage.
I also suspect this is the possible reason for the efficacy of SSRI's on some psychiatric disorders. It's not the actual serotonin release - but an antibiotic or antifungal effect of the drug - or the effect of the migration of mast cells which is known to be affected by concentrations of serotonin - that is actual reason that these drugs have an effect. It could also be a combination.
Something resonates with this line of thinking, it is worth looking into definitely. Of course the theory that it is a metabolite rather than the whole compound that causes the proposed anti-fungal/bacterial effect makes this rather impractical to test.. but there is certainly something to be said for the anti-viral potential of Piracetam itself:
Antiviral Activity of Piracetam, Y.M. Centifanto, Tulane University School
of Medicine, New Orleans, Louisiana (USA)
The effect of Piracetam (2-oxo-i pyrrodiline acetamide), a nootropic
drug, on herpes simplex virus (HSV) infections was examined. We found that
HSV replication on Vero cells was totally inhibited by the drug, even when
added 6 hr pi. The drug needed continuous contact with the infected cell
to exert its effect, suggesting a virustatic mode of action. Three types
of experiments were conducted for the in vivo studies: i) In the hairless
guinea pig model of herpetic recurrent disease, cellophane stripping of a
previously infected area induces the appearance of recurrent herpetic
lesions. Topical application of a 10% Piracetam to these areas inhibited
lesion formation by 70% as compared to the control; 2) Using the same system,
the drug at 20 mg/kg was given either orally or in the drinking water,
prevented lesion formation; 3) Female guinea pigs were infected in the
genital area with HSV-I (333) strain. After the primary lesions subsided,
and in the period of spontaneous recurrent lesions, the animals were given
oral doses of Piracetam for three consecutive weeks. We found that the
drug was effective in reducing the number of recurrent lesions on the
treated animals by more than 50%. Additional experiments with different
doses are now in progress. It is important to note that Piracetam has a
more definite inhibitory action on recurrent lesions as compared to a very
mild action on primary disease. We theorize that this beneficial effect on
the prevention of recurrent lesions may be related to their reported
cholinergic functions.
From: http://brainmeta.com...showtopic=18310
LongeCity
