Apolipoprotein E, amyloid-beta, and neuroinflammation in Alzheimer's disease

  1. Get@NRC: Apolipoprotein E, amyloid-beta, and neuroinflammation in Alzheimer's disease (Opens in a new window)
DOIResolve DOI: http://doi.org/10.1007/s12264-013-1422-z
AuthorSearch for: ; Search for: ; Search for: ; Search for: ; Search for:
Journal titleNeuroscience Bulletin
Pages317330; # of pages: 14
Subjectamyloid beta protein; apolipoprotein E; apolipoprotein E2; apolipoprotein E3; apolipoprotein E4; lipopolysaccharide; Alzheimer disease; cell type; cholesterol transport; disease predisposition; human; nerve cell; nerve cell necrosis; nerve degeneration; nervous system inflammation; neuropathology; nonhuman; review; risk factor; synapse
AbstractAlzheimer's disease (AD) is characterized by the accumulation and deposition of amyloid-beta (Aβ) peptides in the brain. Neuroinflammation occurs in the AD brain and plays a critical role in the neurodegenerative pathology. Particularly, Aβ evokes an inflammatory response that leads to synaptic dysfunction, neuronal death, and neurodegeneration. Apolipoprotein E (ApoE) proteins are involved in cholesterol transport, Aβ binding and clearance, and synaptic functions in the brain. The ApoE4 isoform is a key risk factor for AD, while the ApoE2 isoform has a neuroprotective effect. However, studies have reached different conclusions about the roles of the isoforms; some show that both ApoE3 and ApoE4 have anti-inflammatory effects, while others show that ApoE4 causes a predisposition to inflammation or promotes an inflammatory response following lipopolysaccharide treatment. These discrepancies may result from the differences in models, cell types, experimental conditions, and inflammatory stimuli used. Further, little was known about the role of ApoE isoforms in the Aβ-induced inflammatory response and in the neuroinflammation of AD. Our recent work showed that ApoE isoforms differentially regulate and modify the Aβ-induced inflammatory response in neural cells, with ApoE2 suppressing and ApoE4 promoting the response. In this article, we review the roles, mechanisms, and interrelations among Aβ, ApoE, and neuroinflammation in AD. © 2014 Shanghai Institutes for Biological Sciences, CAS and Springer-Verlag.
Publication date
AffiliationNational Research Council Canada (NRC-CNRC); Human Health Therapeutics (HHT-TSH)
Peer reviewedYes
NPARC number21272114
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Record identifier5dd31774-9d6d-4dc2-a968-bc78928aba4a
Record created2014-07-23
Record modified2016-05-09
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