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The Role of Apolipoprotein E in Alzheimer's Disease

The ɛ4 allele of apolipoprotein E ( APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, pr... Full description

Journal Title: Neuron 2009, Vol.63 (3), p.287-303
Main Author: Kim, Jungsu
Other Authors: Basak, Jacob M , Holtzman, David M
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 0896-6273
Link: https://www.ncbi.nlm.nih.gov/pubmed/19679070
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3044446
title: The Role of Apolipoprotein E in Alzheimer's Disease
format: Article
creator:
  • Kim, Jungsu
  • Basak, Jacob M
  • Holtzman, David M
subjects:
  • Alzheimer Disease - genetics
  • Alzheimer Disease - metabolism
  • Alzheimer Disease - physiopathology
  • Alzheimer's disease
  • Alzheimers disease
  • Amyloid beta-Peptides - metabolism
  • Animals
  • Apolipoproteins
  • Apolipoproteins E - genetics
  • Apolipoproteins E - metabolism
  • Article
  • Blood-brain barrier
  • Brain
  • Brain - metabolism
  • Cholesterol
  • Humans
  • lipids (amino acids
  • Lipoproteins
  • Metabolism
  • Mice
  • Military towns
  • Models, Biological
  • Mutation
  • Neuroscience(all)
  • Pathogenesis
  • peptides
  • proteins
  • Risk factors
ispartof: Neuron, 2009, Vol.63 (3), p.287-303
description: The ɛ4 allele of apolipoprotein E ( APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, prevailing evidence suggests that the differential effects of apoE isoforms on Aβ aggregation and clearance play the major role in AD pathogenesis. Other potential mechanisms, such as the differential modulation of neurotoxicity and tau phosphorylation by apoE isoforms as well as its role in synaptic plasticity and neuroinflammation, have not been ruled out. Inconsistent results among studies have made it difficult to define whether the APOE ɛ4 allele represents a gain of toxic function, a loss of neuroprotective function, or both. Therapeutic strategies based on apoE propose to reduce the toxic effects of apoE4 or to restore the physiological, protective functions of apoE.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0896-6273
fulltext: fulltext
issn:
  • 0896-6273
  • 1097-4199
url: Link


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descriptionThe ɛ4 allele of apolipoprotein E ( APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, prevailing evidence suggests that the differential effects of apoE isoforms on Aβ aggregation and clearance play the major role in AD pathogenesis. Other potential mechanisms, such as the differential modulation of neurotoxicity and tau phosphorylation by apoE isoforms as well as its role in synaptic plasticity and neuroinflammation, have not been ruled out. Inconsistent results among studies have made it difficult to define whether the APOE ɛ4 allele represents a gain of toxic function, a loss of neuroprotective function, or both. Therapeutic strategies based on apoE propose to reduce the toxic effects of apoE4 or to restore the physiological, protective functions of apoE.
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subjectAlzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Alzheimers disease ; Amyloid beta-Peptides - metabolism ; Animals ; Apolipoproteins ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Article ; Blood-brain barrier ; Brain ; Brain - metabolism ; Cholesterol ; Humans ; lipids (amino acids ; Lipoproteins ; Metabolism ; Mice ; Military towns ; Models, Biological ; Mutation ; Neuroscience(all) ; Pathogenesis ; peptides ; proteins ; Risk factors
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abstractThe ɛ4 allele of apolipoprotein E ( APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, prevailing evidence suggests that the differential effects of apoE isoforms on Aβ aggregation and clearance play the major role in AD pathogenesis. Other potential mechanisms, such as the differential modulation of neurotoxicity and tau phosphorylation by apoE isoforms as well as its role in synaptic plasticity and neuroinflammation, have not been ruled out. Inconsistent results among studies have made it difficult to define whether the APOE ɛ4 allele represents a gain of toxic function, a loss of neuroprotective function, or both. Therapeutic strategies based on apoE propose to reduce the toxic effects of apoE4 or to restore the physiological, protective functions of apoE.
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doi10.1016/j.neuron.2009.06.026
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