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Piracetam (UCB-6215) is a cyclic derivative of the neurotransmitter gamma-aminobutyric acid (GABA), used in treatment of a wide range of cognitive disorders.

Piracetam (UCB-6215) is able to significantly decrease the fusogenic and destabilising effect of Abeta 29-42, in a concentration-dependent manner. Preincubation of piracetam, at a piracetam/peptide ratio of 960, during 20 min before the addition of Abeta 29-42 prevents almost completely the mixture of the two fluorescent probes. Preincubation of piracetam with lipids prevents almost completely the release of calcein induced by the peptide in a dose-dependent fashion (piracetam/peptide ratios from 9.6 to 960)[1].

Piracetam (UCB-6215) (< 1.0 mM) preincubated with brain membranes enhances membrane fluidity in aged mice, rats and humans, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam (UCB-6215) (300 mg/kg once daily) significantly increases membrane fluidity in some brain regions of young and aged rats, but has no measurable effect on membrane fluidity in the young rats[2]. Piracetam (UCB-6215) (300 mg/kg daily for 6 weeks) improves active avoidance learning in the aged rats only and elevates membrane fluidity in all brain regions except the cerebellum in the aged rats. Piracetam (UCB-6215) (300 mg/kg daily for 6 weeks) also improves NMDA receptor density in the hippocampus and on muscarinic cholinergic receptor densities in the frontal cortex and the striatum and to a lesser extent in the hippocampus of rats[3].

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