Neuropathobiology of Senile Dementia and Mechanism of Action of Nootropic Drugs

Abstract

Recent advances in neuroscience and molecular neurochemistry have substantially increased the knowledge of the neuropathobiology of senile dementia and Alzheimer's disease. On the basis of various hypotheses concerning degenerative processes in aging brains, new therapeutic strategies have been developed, including nootropic drugs with different mechanisms of action and heterogenous chemical structures. Mutual relationships exist between neuroscientific research and nootropic drug development. To date, such areas of research and drug development have involved deficits of brain neurotransmission (cholinergic, monoaminergic, peptidergic), free radical-induced damage, disturbances of calcium homeostasis and excitatory amino acid function, and deposition of amyloid protein.

Establishing Natural Nootropics: Recent Molecular Enhancement Influenced by Natural Nootropic

“…Piracetam or 2-oxo-1-pyrrolidineacetamide, a cyclic derivative of gamma-aminobutyric acid (GABA) [ 78 ], is widely used in treating senile dementia and Alzheimer's disease [ 79 ]. Studies showed the role of piracetam in enhancing the memory and learning [ 80 ] and act synergistically with choline leading to greater enhancement of cognition.…”

Effects of piracetam on pentylenetetrazol-kindling development, hippocampal potentiation phenomena and kindling-induced learning deficit

“…Nootropic drugs have improving effects on learning and memory in rodents, accelerate the restitution of impaired brain metabolism and neuronal membrane dysfunctions and protect the homeostatic capability of neural cells against various physical and chemical intoxications (Giurgea 1972;Nicholson 1990;Benesova 1994). Various different biochemical and behavioural results have been reported for piracetam and piracetam-like compounds.…”

Cyclic GTP imitates the potentiating effect of the nootrope vinpocetine on the high-threshold A-current in mollusk neurons

“…The other reported studies of the mechanisms of activation of Ca2+-dependent K + currents by the secreted segment of the ffamyloid peptide precursor [8]. This segment, unlike ~-amyloid peptide itself, has neuroprotective properties [5]. Activation of the K + current by this segment, as in our experiments, was mediated by cGME However, unlike the present report, the authors associated the action of cGMP not with a decrease in the cAMP level, but with activation of protein phosphatase.…”