The presence of apoE4, not the absence of apoE3, contributes to AD pathology

Teter, Bruce; Raber, Jacob; Nathan, Britto; Crutcher, Keith A.

doi:10.3233/jad-2002-4305

Cited by 37Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The presence of apoE4, not the absence of apoE3, contributes to AD pathology

Teter, Bruce, Raber, Jacob, Nathan, Britto, Crutcher, Keith A.·2002·Journal of Alzheimer's Disease

DOI 10.3233/jad-2002-4305

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Abstract

ApoE is a component of several classes of lipoproteins regulating lipid metabolism and redistribution [42] and is detected primarily in astrocytes in rodents and in astrocytes and neurons in humans [7,26, 51]. Neuronal apoE levels increase after CNS injuries in humans and rodents [33,38]. The three human isoforms, E2, E3, and E4, (alleles e2, e3, e4) differ by cysteines at two positions (112 and 158) [92]. All other mammalian apoE is E4-like at these cysteine residues, but numerous other differences exist, particularly in the C-terminus, such that rodent apoE cannot be equated with any particular human apoE isoform in its sequence [94]. This is an important consideration when attempting to compare effects of mouse and human apoE in transgenic models. ApoE isoform-specific activities could impact neuronal function through several direct and indirect mechanisms [84], raising the possibility that apoE isoforms differ in the mechanism by which they impact AD pathology [73]. Since the position defended here is that the presence of E4 confers greater risk of AD, an appropriate question is how selection for such a risk factor might occur. The E3 allele has risen to prominence in the last

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There has been intense debate as to whether potential Alzheimer's disease therapeutics should increase or decrease apoE levels.
“There has been intense debate as to whether potential AD therapeutics should increase or decrease apoE levels (Ashford, 2002; Rebeck et al., 2002; Teter et al., 2002; Osherovich, 2009).”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Teter et al., 2002
There is still debate regarding whether increasing or decreasing apoE is the best strategy in regard to AD therapeutics.
“The role of apoE in AD pathogenesis has been studied extensively, but there is still debate regarding whether increasing or decreasing apoE is the best strategy in regard to AD therapeutics (Ashford, 2002;Teter et al., 2002).”
From Anti-ApoE Antibody Given after Plaque Onset Decreases Aβ Accumulation and Improves Brain Function in a Mouse Model of Aβ Amyloidosis (2014) · cites this paper as Teter et al., 2002

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Apolipoprotein E Polymorphism Is Associated with Both Senile Plaque Load and Alzheimer‐Type Neurofibrillary Tangle Formationa
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Untitled work
Cole (2000) · doi:10.1002/1097-0029(20000815)50:4

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“There has been intense debate as to whether potential AD therapeutics should increase or decrease apoE levels (Ashford, 2002; Rebeck et al., 2002; Teter et al., 2002; Osherovich, 2009).”
Background
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“The role of apoE in AD pathogenesis has been studied extensively, but there is still debate regarding whether increasing or decreasing apoE is the best strategy in regard to AD therapeutics (Ashford, 2002; Teter et al., 2002).”
Background
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HaploinsufficiencyofHumanAPOEReducesAmyloid DepositioninaMouseModelofAmyloid-Amyloidosis
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Self-citation

Authors: Teter, B., Raber, J., Nathan, B., & Crutcher, K. A.
Affiliations: University of California, Los Angeles (US)
Oregon Health & Science University (US)
Eastern Illinois University (US)
University of Cincinnati Medical Center (US)
Corresponding author: Teter, Bruce
ORCID: Teter, Bruce
Raber, Jacob
Nathan, Britto
Crutcher, Keith A.
Venue: Journal of Alzheimer's Disease
Publisher: SAGE Publications
Published: 2002-07-24
Volume: 4
Issue: 3
Pages: 155-163
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-2002-4305
OpenAlex: W1460005622
Cited by: 37
References: 94
Citations by year: 2024: 1 · 2021: 1 · 2018: 1 · 2016: 2 · 2015: 1 · 2014: 4 · 2013: 1 · 2012: 2
FWCI: 2.60
Type: journal article
Language: en
Open access: closed
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed (publishedVersion)
The Keep (Eastern Illinois University) (submittedVersion)
Funders: National Institute on Aging (K01AG000962)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: apolipoprotein E, APOE ε4
MeSH terms: Alzheimer Disease, Animals, Apolipoproteins E, Astrocytes, Brain, Humans, Mice, Transgenic, Neurons, Gene Expression, Mice, Apolipoprotein E3, Apolipoprotein E4

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The presence of apoE4, not the absence of apoE3, contributes to AD pathology

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