Alzheimer's disease (AD), the most common cause of dementia in the elderly, is characterized by amyloid β (Aβ)-containing plaques and neurofibrillary tangles, and synaptic and neuronal loss, along with progressive cognitive impairment. Although growing evidence suggests the beneficial effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) on AD, this notion is still controversial. To evaluate the efficacy of statins for Aβ-induced cognitive impairment, we employed an Aβ injection model. Using this model, the present study demonstrated that pretreatment with fluvastatin, but not post-treatment just after Aβ exposure, prevented Aβ-induced memory impairment. We also observed that fluvastatin significantly decreased Aβ accumulation and oxidative stress after Aβ injection. Mice treated with simvastatin, but not fluvastatin, did not demonstrate the prevention of Aβ-induced memory impairment, and showed no significant decrease in oxidative stress. More importantly, fluvastatin significantly prevented the loss of neurons in the basal forebrain induced by Aβ. Overall, the present study demonstrated that fluvastatin significantly prevented memory impairment induced by Aβ. The beneficial effects of fluvastatin might be explained by the preservation of neurons through a significant decrease in Aβ accumulation and oxidative stress. In clinical practice, the timing of the start of fluvastatin treatment might be critical in achieving a beneficial effect on cognitive function.

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