introduction / background

Neurodegenerative diseases are a common cause of morbidity and mortality worldwide with oxidative stress, inflammation and protein aggregation represent the main underlying mechanisms that ultimately lead to cell death. Ethanol has shown strong neurodegenerativ consequences in experimental animal brains. Statins are a class of lipid-lowering drugs with many pleotropic effects.


the aim of the present study was to explore the modulatory effect of simvastatin (10 mg/kg/day) before and after the development of neurodegeneration (for 55 and 25 days, respectively) on redox state, caspase-3 expression, p-protein kinase B (p-Akt) and brain derived neurotrophic factor (BDNF) in ethanol (15%ethanol solution for 55 day) induced neurodegeneration.

Materials & Methods

Seventy female Albino Swiss mice were included and randomly divided into 5 groups: control (c) group; ethanol (E) group; (ES) group treated with simvastatin from the first day of ethanol intake; (E+S) group treated with simvastatin after neurodegeneration development; and simvastatin (S) group.


Administration of simvastatin from the first day improved the biochemical changes, suppressed apoptosis, induced autophagy and neurogenesis. However, its administration after the development of neurodegeneration resulted in partial improvement. The histopathological findings confirmed the biochemical changes.


Simvastatin might have a neuroprotective role via improving redox status, stimulation of neurogenesis, induction of autophagy and the suppression of apoptosis. Thus, the use of simvastatin for protection against the development and progression of neurodegeneration seem to be promising.


Neurodegeneration; simvastatin; oxidative stress; apoptosis; autophagy; neurogenesis.

acknowledgement / Contact

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