Journal
ALZHEIMERS & DEMENTIA
Volume 12, Issue 6, Pages 719-732Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2016.02.010
Keywords
Alzheimer's; Microglia; Neuroinflammation; Neurodegeneration; Systemic inflammation; PET
Categories
Funding
- MRC [G84/6523] Funding Source: UKRI
- Alzheimers Research UK [ARUK-PCRF2014A-1] Funding Source: researchfish
- Medical Research Council [G84/6523] Funding Source: Medline
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Several attempts have been made to treat Alzheimer's disease (AD) using anti-amyloid strategies with disappointing results. It is clear that the amyloid cascade hypothesis alone cannot fully explain the neuronal damage in AD, as evidenced both by autopsy and imaging studies. Neuroinflammation plays a significant role in neurodegenerative diseases, whereas the debate is ongoing about its precise role, whether it is protective or harmful. In this review, we focus on the potential mechanism of glial activation and how local and systemic factors influence disease progression. We focus on neuroinflammation in AD, especially in the earliest stages, a vicious cycle of glial priming, release of proinflammatory factors, and neuronal damage. We review the evidence from imaging studies, regarding the temporal relationship between amyloid deposition and neuroinflammation, the influence of systemic inflammation on glial activation, both in acute and chronic stimulation and the relevance of inflammation as a diagnostic and therapeutic target. (C) 2016 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
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