The immune system on the TRAIL of Alzheimer's disease.
Immune response
Neuroinflammation
Proinflammatory cytokines
Regulatory T cells
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
13 Oct 2020
13 Oct 2020
Historique:
received:
26
05
2020
accepted:
28
09
2020
entrez:
14
10
2020
pubmed:
15
10
2020
medline:
6
8
2021
Statut:
epublish
Résumé
Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive degeneration and loss of neurons in specific regions of the central nervous system. Chronic activation of the immune cells resident in the brain, peripheral immune cell trafficking across the blood-brain barrier, and release of inflammatory and neurotoxic factors, appear critical contributors of the neuroinflammatory response that drives the progression of neurodegenerative processes in AD. As the neuro-immune network is impaired in course of AD, this review is aimed to point out the essential supportive role of innate and adaptive immune response either in normal brain as well as in brain recovery from injury. Since a fine-tuning of the immune response appears crucial to ensure proper nervous system functioning, we focused on the role of the TNF superfamily member, TNF-related apoptosis-inducing ligand (TRAIL), which modulates both the innate and adaptive immune response in the pathogenesis of several immunological disorders and, in particular, in AD-related neuroinflammation. We here summarized mounting evidence of potential involvement of TRAIL signaling in AD pathogenesis, with the aim to provide clearer insights about potential novel therapeutic approaches in AD.
Identifiants
pubmed: 33050925
doi: 10.1186/s12974-020-01968-1
pii: 10.1186/s12974-020-01968-1
pmc: PMC7556967
doi:
Substances chimiques
TNF-Related Apoptosis-Inducing Ligand
0
TNFSF10 protein, human
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
298Subventions
Organisme : PRIN grant from the Italian Ministry of Research
ID : 2017YH3SXK
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