The effects of statins on microglial cells to protect against neurodegenerative disorders: A mechanistic review.

Microglia are the primary innate immune system cells in the central nervous system (CNS). They are crucial for the immunity, neurogenesis, synaptogenesis, neurotrophic support, phagocytosis of cellular debris, and maintaining the CNS integrity and homeostasis. Invasion by pathogens as well as in CNS injuries and damages results in activation of microglia known as microgliosis. The activated microglia have the capacity to release proinflammatory mediators leading to neuroinflammation. However, uncontrolled neuroinflammation can give rise to various neurological disorders (NDs), especially the neurodegenerative diseases including Parkinson's disease (PD) and related disorders, Alzheimer's disease (AD) and other dementias, multiple sclerosis (MS), Huntington's disease (HD), spinocerebellar ataxia (SCA), spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS), and stroke. Statins (HMG-CoA reductase inhibitors) are among the most widely prescribed medications for the management of hypercholesterolemia worldwide. It can be used for primary prevention in healthy individuals who are at higher risk of cardiovascular and coronary heart diseases as well as the secondary prevention in patients with cardiovascular and coronary heart diseases disease. A growing body of evidence has indicated that statins have the potential to attenuate the proinflammatory mediators and subsequent NDs by controlling the microglial activation and consequent reduction in neuroinflammatory mediators. In this review, we have discussed the recent studies on the effects of statins on microglia activation and neuroinflammation.