期刊
MOLECULAR NEURODEGENERATION
卷 17, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s13024-022-00566-4
关键词
Apolipoprotein E; Neuroinflammation; Alzheimer's disease; Neurodegeneration
资金
- Lund University
- Strategic Research Area MultiPark (Multidisciplinary Research in neurodegenerative diseases) at Lund University
- Swedish Alzheimer Foundation
- Swedish Brain Foundation
- Crafoord Foundation
- Swedish Dementia Association
- G&J Kock Foundation
- Olle Engkvist Foundation
- Swedish Medical Research Council
- Swedish Parkinson Foundation
- A.E. Berger Foundation
- Thurings Foundation
- Swedish mental health foundation
- Royal Physiographic Society of Lund
- SYNDEGEN, Marie Curie grant [721802]
- Spanish Ministerio de Ciencia e Innovacion/FEDER/UE [PID2021-124096OB-I00]
- Spanish Junta de Andalucia/FEDER/EU [P18-RT-1372]
- Spanish FEDER I + D+ i-USE [US-1264806]
- Marie Curie Actions (MSCA) [721802] Funding Source: Marie Curie Actions (MSCA)
This article reviews the impact of the APOE genotype on late-onset Alzheimer's disease and central nervous system pathology, covering various factors influencing disease development, such as neuroinflammation, cell function, synaptic function, etc.
ApoE is the major lipid and cholesterol carrier in the CNS. There are three major human polymorphisms, apoE2, apoE3, and apoE4, and the genetic expression of APOE4 is one of the most influential risk factors for the development of late-onset Alzheimer's disease (AD). Neuroinflammation has become the third hallmark of AD, together with Amyloid-beta plaques and neurofibrillary tangles of hyperphosphorylated aggregated tau protein. This review aims to broadly and extensively describe the differential aspects concerning apoE. Starting from the evolution of apoE to how APOE's single-nucleotide polymorphisms affect its structure, function, and involvement during health and disease. This review reflects on how APOE's polymorphisms impact critical aspects of AD pathology, such as the neuroinflammatory response, particularly the effect of APOE on astrocytic and microglial function and microglial dynamics, synaptic function, amyloid-beta load, tau pathology, autophagy, and cell-cell communication. We discuss influential factors affecting AD pathology combined with the APOE genotype, such as sex, age, diet, physical exercise, current therapies and clinical trials in the AD field. The impact of the APOE genotype in other neurodegenerative diseases characterized by overt inflammation, e.g., alpha- synucleinopathies and Parkinson's disease, traumatic brain injury, stroke, amyotrophic lateral sclerosis, and multiple sclerosis, is also addressed. Therefore, this review gathers the most relevant findings related to the APOE genotype up to date and its implications on AD and CNS pathologies to provide a deeper understanding of the knowledge in the APOE field.
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