Neuroinflammation as a Potential Therapeutic Target in Alzheimer’s Disease

Although amyloid-β (Aβ) peptide accumulation is considered as a key early event in the pathogenesis of Alzheimer's disease (AD), the precise pathophysiology of this deadly illness remains unclear and no effective remedies capable of inhibiting disease progression have been discovered. In additi...

Full description

Saved in:
Bibliographic Details
Published inClinical interventions in aging Vol. 17; pp. 665 - 674
Main Authors Liu, Ping, Wang, Yunyun, Sun, Yan, Peng, Guoping
Format Journal Article
LanguageEnglish
Published New Zealand Dove Medical Press Limited 31.05.2022
Dove
Dove Medical Press
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Although amyloid-β (Aβ) peptide accumulation is considered as a key early event in the pathogenesis of Alzheimer's disease (AD), the precise pathophysiology of this deadly illness remains unclear and no effective remedies capable of inhibiting disease progression have been discovered. In addition to deposition of extracellular Aβ plaques and intracellular neurofibrillary tangles, neuroinflammation has been identified as the third core characteristic crucial in the pathogenesis of AD. More and more evidence from laboratory and clinical studies have suggested that anti-inflammatory treatments could defer or prevent the occurrence of AD. In this review, we will discuss multifaceted evidence of neuroinflammation presented in AD and the newly emerged anti-inflammatory targets both in pre-clinical and clinical AD.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1178-1998
1176-9092
1178-1998
DOI:10.2147/CIA.S357558