Modern concepts of alzheimer’s disease pathogenesis: Novel approaches to pharmacotherapy (review)

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Abstract

The review concerns the novel approaches to Alzheimer’s disease pathogenesis represented in modern scientific literature, and aims at studying new possible targets for targeted pharmacotherapy of different stages of neurodegeneration. The multi-factorial disease results in disability and the loss of memory and cognitive functions causing life quality deterioration and the loss of legal capacity. The situation seems to be critical due to the fact that the majority of approved pharmaceuticals have just a symptomatic action rather than an adequate effect. For this reason there is the search for new target molecules for pharmacological intervention. Moreover, novel pharmaceuticals with more selective effect are being developed now. Modern concepts of Alzheimer’s disease pathogenesis are based on the recognized significance of the following pathological processes: neuronal damage and death, impaired neurogenesis and cell-to-cell interactions, neuroinflammation and vasculopathy development, while the accumulation of damaged proteins can be both a trigger mechanism, and also the result of the mentioned events. Based on the above stated ideas, there being developed the pharmacological approaches aimed at preventing pathologically damaged proteins from accumulating in brain, arresting aberrant neurotransmission, the correction of neuroinflammation and impaired neurogenesis, as well as the recovery of cell-to-cell interactions. The use of adequate animal models of Alzheimer’s disease is one of promising approaches to the development of novel pharmacotherapeutical strategies.

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Komleva, Y. K., Kuvacheva, N. V., Lopatina, O. L., Gorina, Y. V., Frolova, O. V., Teplyashina, E. A., … Salmina, A. B. (2015, September 29). Modern concepts of alzheimer’s disease pathogenesis: Novel approaches to pharmacotherapy (review). Sovremennye Tehnologii v Medicine. Nizhny Novgorod State Medical Academy. https://doi.org/10.17691/stm2015.7.3.19

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