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Gene Transfer of Human Apoe Isoforms Results in Differential Modulation of Amyloid Deposition and Neurotoxicity in Mouse Brain
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Introduction of different APOE isoforms modulates Aβ peptide aggregation and neurotoxicity after amyloid deposition in mouse brain.
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“Based on these observations, one strategy to prevent AD in APOE4 carriers is to modify the central nervous system (CNS) genetically to express APOE2, providing the CNS with the protective APOE2 to balance the AD risk associated with expression of APOE4.22–26”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [24]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Previous studies using homozygous APOE knock-in mice have been essential for de fi ning isoform-speci fi c effects of APOE2 , APOE3 , and APOE4”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [33]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Moving in vivo, other studies have explored vector-mediated delivery to supplement the E4 brain with neuroprotective E2 protein, showing that exogenous E2 markedly decreases amyloid burden in mice9–12.”
From APOE4 to APOE2 allelic switching in mice improves Alzheimer’s disease-related metabolic signatures, neuropathology and cognition (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Expression of apoE3 and apoE4 in the mouse brain results in diminished efflux of A into the blood compared with apoE2 (Hudry et al., 2013).”
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 Hudry et al., 2013
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“overexpression of human APOE ε2 allele in APP/PS1 mice was able to attenuate brain Aβ oligomerization and plaque deposition, as well as peri-plaque synapse loss and neurite dystrophy, in contrast to the injection of ApoE4-encoding AAVs [79].”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [79]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“M-apoE and h-apoE differ in both structure [119] and functions ranging from lipid binding and transport, to effects on AD pathology [22, 84, 85, 119, 120].”
From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [120]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The protective effect of APOE2 genetic modification of the CNS was replicated by Hudry et al.24 using an adeno-associated virus serotype 4 (AAV4) vector to deliver APOE2 into the cerebrospinal fluid (CSF) of the lateral ventricle of mice overexpressing a mutant β-amyloid precursor protein (APP) transgene”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“The efficacy of this approach in AD transgenic mouse models has been demonstrated previously.23,24,26”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“while viral APOE2 delivery, APOE2 gene therapy, and inducible APOE4 to APOE2 switching have demonstrated that increasing APOE2 expression or replacing APOE4 with APOE2 can ameliorate AD-related phenotypes 7,8,33,34 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [33]
The cited source says what the claim attributes to it.
In the citing paper
“APOE exerts toxic effects on the cerebrovascular system (694) and neurons (383, 384) and influences A 𝛃 clearance (60, 64, 98, 135, 256, 266, 278, 294, 315, 693), amyloid deposition (39, 256, 258, 266, 278, 314, 518, 612), and tau-related neurodegeneration (533) in an allele-dependent manner APOE4 > APOE3 > APOE2 .”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [266]
The cited source says what the claim attributes to it.
In the citing paper
“Epidemiological evidence and evidence from neuropathological assessment of the impact of apoE isoforms on the brain Aβ load, have suggested that apoE2 exerts a protective effect against Aβ pathology and AD morbidity [3,9,10], while apoE4, in contrast, markedly enhances the disease process [7,8,30].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“ApoE plays an important role in amyloidosis progression (Dodart et al., 2005;Hudry et al., 2013).”
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 Hudry et al., 2013
The cited source says what the claim attributes to it.
In the citing paper
“Unlike other two isoforms, apoE2 has not been studies extensively but consistent data appear to support its neuroprotective function (Hudry et al., 2013).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Hudry et al., 2013
The cited source says what the claim attributes to it.
In the citing paper
“These results bear a striking resemblance to those from the Aβ plaque-depositing mice120,128 and indicate that the effect of APOE4 in AD is due not only to the increased propensity of proteins to aggregate in the presence of APOE4, but also to the way APOE4 modulates the brain response to those aggregates once formed.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [128]
The cited source says what the claim attributes to it.
In the citing paper
“The introduction of human APOE2 into plaque-depositing mice expressing endogenous mouse Apoe via AAV-mediated delivery was shown to prevent and even reverse the deposition of Aβ into plaques, whereas delivery of APOE4 had the opposite effect128”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [128]
The cited source says what the claim attributes to it.
In the citing paper
“In general, experiments suggest the order of APOE4 > APOE3 > APOE2 for effects on amyloid deposition (Fagan et al, 2002; Castellano et al, 2011; Hudry et al, 2013; Zhao et al, 2016)”
From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Hudry et al, 2013
The cited source says what the claim attributes to it.
In the citing paper
“This has also been observed with viral-vector mediated overexpression of APOE4 isoforms in AD mouse brains (Dodart et al, 2005; Hudry et al, 2013; Zhao et al, 2016).”
From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Hudry et al, 2013
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“using a previously published split-luciferase complementation assay34”
From Resistance to autosomal dominant Alzheimer’s disease in an APOE3 Christchurch homozygote: a case report (2019) · cites this paper as [34]
Experimental — accuracy not yet measuredIn the citing paper
“While there is data to support the concept that ApoE2 expression may be protective using a gene transfer approach (Hu et al., 2015; Hudry et al., 2013), it would be useful to validate protective effects and lack of toxicity in a number of different models.”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Hudry et al., 2013
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“This finding also aligns with evidence that Aβ oligomer levels in APOE4 AD patients’ brains are 2.7 times higher than those in APOE3 AD patients [73] and is consistent with findings from mouse models expressing APOE4 and APOE2 [74].”
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Metadata
- Authors
- Hudry, E., Dashkoff, J., Roe, A. D., Takeda, S., Koffie, R. M., Hashimoto, T., Scheel, M., Spires-Jones, T., Arbel-Ornath, M., Betensky, R., Davidson, B. L., & Hyman, B. T.
- Affiliations
- MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
- Harvard University (US)
- University of Iowa (US)
- Corresponding author
- Hyman, Bradley T.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2013-11-20
- Volume
- 5
- Issue
- 212
- Pages
- 212ra161-212ra161
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC4334150
- OpenAlex
- W2136199683
- Cited by
- 187
- References
- 55
- Citations by year
- 2026: 8 · 2025: 24 · 2024: 21 · 2023: 12 · 2022: 13 · 2021: 14 · 2020: 15 · 2019: 14 · 2018: 15 · 2017: 5 · 2016: 19 · 2015: 9 · 2014: 18
- FWCI
- 10.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Japan Society for the Promotion of Science (24800015)
- National Institute on Aging (R00AG033670, P50AG005134, 1RC1AG026265-01, R00AG33670, P30AG062421)
- National Institute on Drug Abuse (F32DA026265)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK54759, P30DK054759)
- National Institute of Neurological Disorders and Stroke (NS 34568, R01NS034568)
- National Institute of Environmental Health Sciences (P30ES005605)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-33531, R01HD033531)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- apolipoprotein E, APOE isoforms, APOE ε4, APOE2, Alzheimer's disease, amyloid-beta, synaptotoxicity, amyloid-beta oligomers, amyloid-beta clearance, dystrophic neurites, synaptic loss, gene transfer, transgenic mouse model, genetic risk
- MeSH terms
- Amyloid, Animals, Apolipoproteins E, Brain, Humans, Injections, Intraventricular, Mice, Transgenic, Transfection, Mice
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