Format

Send to

Choose Destination
Alzheimers Dement. 2016 Jun;12(6):719-32. doi: 10.1016/j.jalz.2016.02.010. Epub 2016 May 11.

Neuroinflammation in Alzheimer's disease: Current evidence and future directions.

Author information

1
Neurology Imaging Unit, Imperial College London, UK.
2
Neurology Imaging Unit, Imperial College London, UK. Electronic address: paul.edison@imperial.ac.uk.

Abstract

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 pro-inflammatory 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.

KEYWORDS:

Alzheimer's; Microglia; Neurodegeneration; Neuroinflammation; PET; Systemic inflammation

PMID:
27179961
DOI:
10.1016/j.jalz.2016.02.010
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center