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Annu Rev Med. 2018 Jan 29;69:437-449. doi: 10.1146/annurev-med-050715-104343. Epub 2017 Nov 6.

Innate Immunity and Neurodegeneration.

Labzin LI1, Heneka MT2,3,4, Latz E5,3,4,6.

Author information

1
Division of Protein and Nucleic Acid Chemistry, MRC Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom; email: llabzin@mrc-lmb.cam.ac.uk.
2
Department of Neurodegenerative Disease and Gerontopsychiatry/Neurology, University Hospitals Bonn, Bonn 53127, Germany; email: Michael.Heneka@ukb.uni-bonn.de.
3
Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
4
German Center for Neurodegenerative Diseases, Bonn 53175, Germany.
5
Institute of Innate Immunity, University Hospitals Bonn, Bonn 53127, Germany; email: eicke.latz@uni-bonn.de.
6
Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim 7491, Norway.

Abstract

The innate immune system plays diverse roles in health and disease. It represents the first line of defense against infection and is involved in tissue repair, wound healing, and clearance of apoptotic cells and cellular debris. Excessive or nonresolving innate immune activation can lead to systemic or local inflammatory complications and cause or contribute to the development of inflammatory diseases. In the brain, microglia represent the key innate immune cells, which are involved in brain development, brain maturation, and homeostasis. Impaired microglial function, either through aberrant activation or decreased functionality, can occur during aging and during neurodegeneration, and the resulting inflammation is thought to contribute to neurodegenerative diseases. This review highlights recent advances in our understanding of the influence of innate immunity on neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease.

KEYWORDS:

Alzheimer's disease; Huntington's disease; Parkinson's disease; Toll-like receptors; amyotrophic lateral sclerosis; inflammasomes; neuroinflammation

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