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Alzheimer's disease (AD), a severe form of senile dementia is a neurodegenerative disorder. One of the most well characterized hallmarks of AD are extra-neuronal aggregates of amyloid-beta peptide (A ), known as amyloid plaques. Recent epidemiological studies suggest a link between statin intake, and a lowered incidence of AD. Statins are 3-hydroxy-3-methylglutaryl co-enzyme reductase (HMG) inhibitors, which are one of the most commonly prescribed drug groups used to lower serum cholesterol levels in patients with heart disease. Some of the pleiotropic effects of statins which are gaining attention are its ability to reduce A production and deposition, inhibit caspase-3 mediated apoptosis, and demonstrate anti-inflammatory properties by reducing interleukin-6 (IL-6) levels. The molecular mechanisms responsible for the pleiotropic effects of statins in promoting neuronal survival are not fully understood. Our own research has shown that statins promote anti-apoptotic responses against A -neurotoxicity through -catenin-TCF/LEF signaling however, other anti-apoptotic statin mediated signaling pathways may also be involved. This review will describe AD pathogenesis, A production, and the role of statins in mitigating these effects.