PMC:2944646 / 32370-34427
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/2944646","sourcedb":"PMC","sourceid":"2944646","source_url":"https://www.ncbi.nlm.nih.gov/pmc/2944646","text":"Two older studies have investigated the cognition improving effects of piracetam in young volunteers under mild hypoxia as a pharmacological model to mirror impaired brain function as seen in aging or dementia (Demay and Bande, 1980; Saletu et al., 1995). The data from Demay and Bande (1980) are given in Figure 5 showing considerably less errors in a memory task under hypoxia following 5 days of piracetam treatment with 4.8 g per day, the average therapeutic dose even used today (Figure 5). Hypoxia induced cognitive but also biochemical and physiological deficits mirroring the situation in dementia has also been used in a very recent study in rats (He et al., 2008). In this study, chronic cerebral hyperfusion was induced by ligature of bilateral common carotid arteries leading to acute but also subacute structural and functional brain deficits. Most importantly, spatial memory performance (Morris Water maze) was substantially impaired and showed pronounced improvement by piracetam treatment (600 mg) per day starting after surgery (Figure 6). Besides reducing histopathologic markers of neuronal damage and reducing the expression of proapoptotic proteins, piracetam also improved long term potentiation in the CA3 region of the hippocampus of lesioned animals (Figure 7). Together with data that piracetam reduces neuronal loss and improves synaptic reorganization after chronic alcohol consumption (Brandao et al., 1995; Brandao et al., 1996) with findings of enhanced restitution and reorganization of cortical neuronal circuits after brain damage (Coq and Xerri, 1999; Xerri and Zennou-Azogui, 2003), and with findings that piracetam improves neuritic outgrowth after oxidative stress and/or Aß mediated stress (Kurz et al., 2010), the findings of He et al. (2008) strongly support the concept that piracetam given chronically might improve many parameters of synaptic plasticity from LTP at the synaptic level, to enhanced neurite- as well as synaptogenesis at the structural level, and may even partially protect neurons from 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