Manipulation of Microglial Activation as a Therapeutic Strategy in Alzheimers Disease

Title: Manipulation of Microglial Activation as a Therapeutic Strategy in Alzheimers Disease

Volume: 14 Issue: 27

Author(s): Feng-Shiun Shie and Randall L. Woltjer

Affiliation:

Keywords: Alzheimer's disease, microglial activation, neuroinflammation, beta-amyloid, tau, therapy

Abstract: Alzheimers disease (AD) is the leading cause of dementia. Although the etiology of AD remains controversial, the amyloid hypothesis suggests that β-amyloid (Aβ) peptides may contribute to brain dysfunction, and microglial activation has become increasingly regarded as a potential contributor to disease pathogenesis. Microglial activation is characterized by morphological changes and by production of various effectors, and activated neuroinflammation concurrent with increased oxidative stress may contribute to damage to neurons. However, recently there has been a recognition that microglia may also play a neuroprotective role through their release of neurotrophic factors and through phagocytosis of Aβ. Thus, there is growing consensus that a favorable combination of diminished microglia- mediated neuroinflammation and enhanced Aβ clearance may be critical in AD therapy. In this review, we will discuss the role of microglial activation in AD and how pharmacologic manipulation of microglia might bear upon the treatment of AD.

Cite this article as:

Shie Feng-Shiun and Woltjer L. Randall, Manipulation of Microglial Activation as a Therapeutic Strategy in Alzheimers Disease, Current Medicinal Chemistry 2007; 14 (27) . https://dx.doi.org/10.2174/092986707782359981