Autophagy Balances Neuroinflammation in Alzheimer’s Disease

Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as intracellular pathogens for energy and survival. Dysfunction of autophagy has been associated with the pathologies of Alzheimer’s disease (AD), including...

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Published inCellular and molecular neurobiology Vol. 43; no. 4; pp. 1537 - 1549
Main Authors Cheng, Xuehua, Wei, Yong, Qian, Zijun, Han, Li
Format Journal Article
LanguageEnglish
Published New York Springer US 01.05.2023
Springer Nature B.V
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Abstract Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as intracellular pathogens for energy and survival. Dysfunction of autophagy has been associated with the pathologies of Alzheimer’s disease (AD), including Aβ plaques and neurofibrillary tangles. Recently, the presence of sustained immune response in the brain has been considered a new core pathology in AD. Accumulating evidence suggests that autophagy activation may suppress inflammation response through degrading inflammasomes or pro-inflammatory cytokines and improving immune system function in both clinical trials and preclinical studies. This review provides an overview of updated information on autophagy and inflammation and their potential mediators in AD. In summary, we believe that understanding the relationship between autophagy and inflammation will provide insightful knowledge for future therapeutic implications in AD.
AbstractList Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as intracellular pathogens for energy and survival. Dysfunction of autophagy has been associated with the pathologies of Alzheimer’s disease (AD), including Aβ plaques and neurofibrillary tangles. Recently, the presence of sustained immune response in the brain has been considered a new core pathology in AD. Accumulating evidence suggests that autophagy activation may suppress inflammation response through degrading inflammasomes or pro-inflammatory cytokines and improving immune system function in both clinical trials and preclinical studies. This review provides an overview of updated information on autophagy and inflammation and their potential mediators in AD. In summary, we believe that understanding the relationship between autophagy and inflammation will provide insightful knowledge for future therapeutic implications in AD.
Author Cheng, Xuehua
Qian, Zijun
Wei, Yong
Han, Li
Author_xml – sequence: 1
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  orcidid: 0000-0002-7481-9495
  surname: Cheng
  fullname: Cheng, Xuehua
  organization: Department of TCM Geriatrics, Huadong Hospital Affiliated to Fudan University
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  orcidid: 0000-0002-3506-7921
  surname: Wei
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  givenname: Zijun
  orcidid: 0000-0002-8512-6889
  surname: Qian
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  organization: Shanghai Municipal Hospital of Traditional Chinese Medicine
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  givenname: Li
  surname: Han
  fullname: Han, Li
  email: tcmtoto@163.com
  organization: Department of TCM Geriatrics, Huadong Hospital Affiliated to Fudan University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35960407$$D View this record in MEDLINE/PubMed
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Keywords Inflammation
NLRP3 inflammasomes
Genetic factors
Alzheimer’s disease
Autophagy
Microglia
Language English
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Snippet Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as...
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SubjectTerms Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Autophagy
Biomedical and Life Sciences
Biomedicine
Cell Biology
Clinical trials
Evolutionary conservation
Humans
Immune response
Inflammasomes
Inflammasomes - metabolism
Inflammation
Inflammation - pathology
Macromolecules
Microglia - metabolism
Mitochondria
Neurobiology
Neurodegenerative diseases
Neurofibrillary tangles
Neuroinflammatory Diseases
Neurosciences
Organelles
Review Paper
Senile plaques
Title Autophagy Balances Neuroinflammation in Alzheimer’s Disease
URI https://link.springer.com/article/10.1007/s10571-022-01269-6
https://www.ncbi.nlm.nih.gov/pubmed/35960407
https://www.proquest.com/docview/2797037867
https://search.proquest.com/docview/2702182525
Volume 43
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