HDL-mimetic peptide treatment reverses APOE4-induced transcriptomic and lipidomic alterations in the brain of humanized APOE mice.
Overview
- Graduate Program in Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA
- Department of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, Minnesota, USA
- Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA
Abstract
The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE307255, at NCBI GEO; found in “DATA AVAILABILITY STATEMENT”
Data availability statement
The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:
- it points to a dataset: NCBI GEO GSE307255
Read it in the paper: doi.org/10.1002/alz.71568.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 6 keywords, 15 MeSH terms, 4 funders, 86 references.
Cite
This paper
Chang, A., Kim, M., Glittenberg, M., Qu, W., Li, D., & Li, L. (2026). HDL-mimetic peptide treatment reverses APOE4-induced transcriptomic and lipidomic alterations in the brain of humanized APOE mice. Alzheimer's & dementia : the journal of the Alzheimer's Association, 22(6), e71568. https://
BibTeX
@article{chang2026hdl,
author = {Chang, Allison and Kim, Minwoo and Glittenberg, Matthew and Qu, Wenhui and Li, Danni and Li, Ling},
title = {{HDL-mimetic peptide treatment reverses APOE4-induced transcriptomic and lipidomic alterations in the brain of humanized APOE mice}},
journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
year = {2026},
month = jun,
volume = {22},
number = {6},
pages = {e71568},
publisher = {Wiley},
issn = {1552-5260},
doi = {10.1002/
url = {https://
pmid = {42337953},
pmcid = {PMC13290654}
}
RIS
TY - JOUR
AU - Chang, Allison
AU - Kim, Minwoo
AU - Glittenberg, Matthew
AU - Qu, Wenhui
AU - Li, Danni
AU - Li, Ling
TI - HDL-mimetic peptide treatment reverses APOE4-induced transcriptomic and lipidomic alterations in the brain of humanized APOE mice
T2 - Alzheimer's & dementia : the journal of the Alzheimer's Association
J2 - Alzheimers Dement
PY - 2026
DA - 2026/
VL - 22
IS - 6
SP - e71568
SN - 1552-5260
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "HDL-mimetic peptide treatment reverses APOE4-induced transcriptomic and lipidomic alterations in the brain of humanized APOE mice",
"container-title": "Alzheimer's & dementia : the journal of the Alzheimer's Association",
"author": [
{
"family": "Chang",
"given": "Allison"
},
{
"family": "Kim",
"given": "Minwoo"
},
{
"family": "Glittenberg",
"given": "Matthew"
},
{
"family": "Qu",
"given": "Wenhui"
},
{
"family": "Li",
"given": "Danni"
},
{
"family": "Li",
"given": "Ling"
}
],
"container-title-short":
"volume": "22",
"issue": "6",
"page": "e71568",
"DOI": "10.1002/
"PMID": "42337953",
"PMCID": "PMC13290654",
"ISSN": "1552-5260",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1016/j.isci.2026.115638 [code]
- Genome-scale metabolic modeling uncovers cell-type specific signatures associated with APOE variants.Journal: iScienceIn common: Alzheimer's / dementia, genetics / omics, 5 references
- [2] doi:10.1186/s12974-026-03970-5
- Estrogen deprivation exacerbates Alzheimer's disease pathology through neuronal CTSS signaling.Journal: Journal of neuroinflammationIn common: Alzheimer's / dementia, genetics / omics, mouse, 5 references
- [3] doi:10.1016/j.xcrm.2026.102943 [code]
- Parent-of-origin effects in Alzheimer's liability dissociate neurocognitive and cardiovascular traits in at-risk individuals.Journal: Cell reports. MedicineIn common: Alzheimer's / dementia, clinical / translational, 3 references
- [4] doi:10.1002/advs.202523511
- Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)In common: Alzheimer's / dementia, clinical / translational, genetics / omics, 1 other category, 4 references
- [5] doi:10.3389/fnins.2026.1843319 [code]
- Humanized APOE mouse brain volume increases over age irrespective of sex and APOE genotype: implications for translational validity to the human.Journal: Frontiers in neuroscienceIn common: Alzheimer's / dementia, clinical / translational, genetics / omics, 1 other category, 2 references
- [6] doi:10.1523/eneuro.0468-25.2026 [code]
- A Multi-Network Approach Identifies Proteins Related to Dendritic Spines in Alzheimer's Disease.Journal: eNeuroIn common: Alzheimer's / dementia, genetics / omics, 3 references
- [7] doi:10.1038/s41586-026-10679-1 [code]
- Cortical development dynamics across autism spectrum disorder mouse models.Journal: NatureIn common: genetics / omics, mouse, 4 references
- [8] doi:10.1002/alz.71804
- A meta-refined human Alzheimer's disease-associated gene subset shows partial mouse-model pathway correspondence and limited cross-cohort machine-learning transportability.Journal: Alzheimer's & dementia : the journal of the Alzheimer's AssociationIn common: Alzheimer's / dementia, genetics / omics, mouse, 3 references
- [9] doi:10.1186/s12974-026-03888-y
- Integrated imaging and molecular profiling reveals APOE4-associated neurovascular and glial disruptions in young adult mice.Journal: Journal of neuroinflammationIn common: Alzheimer's / dementia, genetics / omics, mouse, 2 references
- [10] doi:10.1167/iovs.67.10.41
- Ascl1 Represses Müller Glial and Promotes Rod Photoreceptor Fate Through Repressing Notch Signaling in Late Retinal Progenitor Cells.Journal: Investigative ophthalmology & visual scienceIn common: genetics / omics, mouse, 4 references
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
