APOE immunotherapy reduces cerebral amyloid angiopathy and amyloid plaques while improving cerebrovascular function
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Targeting APOE using an anti-APOE antibody ameliorates amyloid pathology while protecting cerebrovascular integrity and function.
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APOE's possible role in Alzheimer's pathophysiology includes cellular mechanisms involving neuronal and glial functions, together with direct effects in Aβ aggregation and deposition.
“APOE’s possible role in Alzheimer’s pathophysiology include cellular mechanisms involving neuronal and glial functions [34, 35], together with direct effects in amyloid-β (Aβ) aggregation and deposition [37].”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [37]
The citation is attached to the claim about Aβ aggregation and deposition, not the preceding neuronal and glial mechanisms. The Discussion (page unavailable) reports that APOE lipidation influences plaque deposition, but says whether poorly lipidated APOE directly seeds Aβ accumulation remains unknown. It therefore supports an effect on deposition, not an established direct effect on aggregation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAn antibody against non-lipidated APOE, which is the version most likely to oligomerize, has shown promise in multiple Alzheimer disease mouse models.
“Along this line, an antibody against non-lipidated APOE, which is the version most likely to oligomerize, has shown promise in multiple AD mouse models136–139.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [137]
The Introduction identifies HAE-4 as an antibody that recognizes poorly lipidated human APOE, and the Results report reduced amyloid pathology and improved vascular function in treated mice. The paper does not say that non-lipidated APOE is the form most likely to oligomerize. Its treatment findings concern a particular mouse model; the sentence’s reference to multiple models is not established by this study alone. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAn antibody that preferentially binds to non-lipidated APOE4 has shown promise in reducing Aβ plaques and CAA in a mouse model of β-amyloidosis, as well as decreasing Aβ-driven tau seeding in mice.
“An antibody that preferentially binds to non-lipidated APOE4 has shown promise in reducing Aβ plaques and CAA in a mouse model of β-amyloidosis, as well as decreasing Aβ-driven tau seeding in mice137–139.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [137]
The Introduction identifies HAE-4 as an antibody that recognizes poorly lipidated human APOE, and the Results report reduced parenchymal Aβ plaques and CAA in APOE4-expressing mice. The Discussion states that these mice do not develop intracellular tau accumulation and that HAE-4’s effect on tau spreading remains unknown; this paper therefore does not support the tau-seeding part of the sentence. (LLM, conf=0.91)
Experimental — accuracy not yet measuredSeveral groups have suggested lowering of APOE expression with APOE-antibodies or using antisense therapy as a therapeutic option for AD.
“Several groups have suggested lowering of APOE expression with APOE-antibodies (Gratuze et al, 2022; Liao et al, 2018; Xiong et al, 2021) or using antisense therapy (Huynh et al, 2017) as a therapeutic option for AD.”
From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Xiong et al, 2021
The Introduction describes HAE-4 as an antibody targeting APOE in amyloid plaques, and the Discussion proposes its therapeutic potential for AD. The paper reports reduced amyloid pathology in mice, not lowered APOE expression. The antisense-therapy clause is attributed to a different citation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredApoE specific immunotherapy against human ApoE reduces CAA.
“while ApoE specific immunotherapy against human ApoE reduces CAA [37]”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [37]
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“Moreover, an association between parenchymal CAA pathology, perivascular tau pathology [36], and neuronal tau pathology severity has been described [27], consistent with this case’s unique pattern of pathology in which the few regions affected with CAA showed also higher tau pathology.”
BackgroundInfluentialAnti-inflammatory clearance of amyloid-β by a chimeric Gas6 fusion protein
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- Authors
- Xiong, M., Jiang, H., Serrano, J. R., Gonzales, E. R., Wang, C., Gratuze, M., Hoyle, R., Bien-Ly, N., Silverman, A. P., Sullivan, P. M., Watts, R. J., Ulrich, J. D., Zipfel, G. J., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Denali Therapeutics, South San Francisco, CA 94080, USA.
- Codexis (United States) (US)
- Duke Medical Center (US)
- Denali Therapeutics (United States) (US)
- Corresponding author
- Holtzman, David M.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2021-02-17
- Volume
- 13
- Issue
- 581
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC8128342
- OpenAlex
- W3129458336
- Cited by
- 179
- References
- 51
- Citations by year
- 2026: 19 · 2025: 40 · 2024: 36 · 2023: 31 · 2022: 39 · 2021: 14
- FWCI
- 19.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute on Aging (AG062027, AG047644, 2P30AG019610)
- NIH Office of the Director (OD021629)
- National Institute of General Medical Sciences (5T32GM008151)
- National Institute of Neurological Disorders and Stroke (NS103276)
- JPB Foundation
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cerebral amyloid angiopathy, amyloid plaques, cerebrovascular dysfunction, microhemorrhages, reactive astrocytes, microglia, neuroinflammation, 5xFAD mice, leptomeningeal arteries, aria
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Brain, Immunotherapy, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Mice, Plaque, Amyloid
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