Dondante
Bluelighter
- Joined
- Dec 6, 2005
- Messages
- 1,638
Sorry to be getting off topic a bit, but I found this interesting article:
http://www.ncbi.nlm.nih.gov/entrez/..._uids=16834757&query_hl=1&itool=pubmed_DocSum
A rehash of what already has been said about Piracetam:
http://www.ncbi.nlm.nih.gov/entrez/..._uids=16007238&query_hl=1&itool=pubmed_DocSum
Article about idebenone (useful, but not double-blind placebo):
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=9706371&query_hl=4&itool=pubmed_DocSum
http://www.ncbi.nlm.nih.gov/entrez/..._uids=16834757&query_hl=1&itool=pubmed_DocSum
DM232 (unifiram) and DM235 (sunifiram) are potent cognition-enhancers, which are four order of magnitude more potent than piracetam. These compounds, although not showing affinity in binding studies for the most important central receptors or channels, are able to prevent amnesia induced by modulation of several neurotransmission systems. These compounds are able to increase the release of acetylcholine from rat cerebral cortex, and, as far as unifiram is concerned, to increase the amplitude of fEPSP in rat hippocampal slices. In vitro experiments, performed on hippocampal slices, also supported the hypothesis of a role of the AMPA receptors for the cognition-enhancing properties of unifiram and sunifiram.
A rehash of what already has been said about Piracetam:
http://www.ncbi.nlm.nih.gov/entrez/..._uids=16007238&query_hl=1&itool=pubmed_DocSum
Piracetam, a derivative of the neurotransmitter gamma-aminobutyric acid (GABA), has a variety of physiological effects that may result, at least in part, from the restoration of cell membrane fluidity. At a neuronal level, piracetam modulates neurotransmission in a range of transmitter systems (including cholinergic and glutamatergic), has neuroprotective and anticonvulsant properties, and improves neuroplasticity. At a vascular level, it appears to reduce erythrocyte adhesion to vascular endothelium, hinder vasospasm, and facilitate microcirculation. This diverse range of physiological effects is consistent with its use in a range of clinical indications. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated.
Article about idebenone (useful, but not double-blind placebo):
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=9706371&query_hl=4&itool=pubmed_DocSum
Within a general cerebral deficit model--inspiratory hypoxia-the dose--effect relationship of idebenone (CAS 58186-27-9), an antioxidant, was studied with regard to selected electrophysiological and psychometric parameters. Seventeen healthy male volunteers (mean age = 32 years, mean BW = 75 kg) received three different oral medications: placebo, idebenone and piracetam (CAS 7491-74-9) as reference. The test drug idebenone was administered in five different dosages, ranging--in 60 mg steps--from 60 to 300 mg t.id. Piracetam was given at a dose level of 800 mg t.i.d. A strict dose-regimen was used in idebenone for safety reasons. Each dosage/medication--except idebenone 300 mg t.i.d.--was given for one week without washouts in between. ... In this pilot study, the target variable, the amplitude of the ERG b-wave indicated a definite antihypoxidotic effect after the highest dosage of idebenone. With 300 mg idebenone t.i.d., ERG b-wave amplitudes increased linearily with increasing duration of treatment. The 'central' AEP P2-amplitude demonstrated a different dose-effect relationship. AEP P2-amplitudes increased with increasing dosages of idebenone. The prolongation of treatment with 300 mg t.i.d. resulted in no further improvement of this parameter (ceiling effect). Subjective ratings (VAS) by the volunteers confirmed the results seen in electrophysiological variables. The findings, however, remain to be confirmed within an adequate double-blind, crossover study design.