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Hindi Review Article
Toll-Like Receptor Signaling in Alzheimer's Disease Progression
Eric J Downer*
Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland
- Corresponding Author:
- Eric J Downer
Department of Anatomy and Neuroscience
Western Gateway Building
University College Cork, Cork, Ireland
Tel: 353-21-4205481
E-mail: edowner@ucc.ie
Received date: February 28, 2013; Accepted date: April 05, 2013; Published date: April 24, 2013
Citation: Downer EJ (2013) Toll-Like Receptor Signaling in Alzheimer’s Disease Progression. J Alzheimers Dis Parkinsonism S10:006. doi:10.4172/2161-0460.S10-006
Copyright: © 2013 Downer EJ. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Evidence continues to underpin the role of the innate immune system in pathologies associated with neuroinflammation. Neuroinflammation is the complex innate immune response of neural tissue to control infection, and Toll-like receptors (TLRs), a major family of pattern recognition receptors (PRRs) that mediate innate immunity, have emerged as players in Alzheimer’s disease (AD). Upon ligation with their ligand, TLRs induce signaling involving recruitment of various adaptors and signaling molecules that culminate in the activation of genes including interferons and cytokines. TLR expression has been identified on resident central nervous system cells including microglia and neurons, with an altered expression profile for this receptor determined in microglia from AD patients. Furthermore, TLR activation on microglia is associated with amyloid-β (Aβ) clearance from the brain, suggesting that modulation of TLR signaling may be a therapeutic strategy for plaque removal. This review will highlight evidence linking the TLR system with the progression of AD, assessing TLR involvement in events associated with AD in cellular systems, transgenic murine models of AD and in humans.
