---
title: "MTHFR 677C>T variant drives prodromal cerebrovascular and synaptic signatures in a mouse model of"
id: "biorxiv-0-mthfr-677c-t-produces-distinct-prodromal-disease-signatures-in-a-mouse-model-of"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-mthfr-677c-t-produces-distinct-prodromal-disease-signatures-in-a-mouse-model-of"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1?rss=1"
published_at: "2026-08-28T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MTHFR 677C>T variant drives prodromal cerebrovascular and synaptic signatures in a mouse model of
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-mthfr-677c-t-produces-distinct-prodromal-disease-signatures-in-a-mouse-model-of
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1?rss=1)
- **Published At:** 2026-08-28T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The MODEL-AD Consortium generated a novel mouse strain combining humanized Alzheimer’s risk alleles (humanized Abeta, **APOEε4**, Trem2*R47H) with homozygosity for the **Mthfr 677C>T** variant on a C57BL/6J background; this strain is referred to as LOAD2.Mthfr677C>T. - The study aimed to assess how the Mthfr677C>T variant contributes to disease-relevant phenotypes in the context of late‑onset Alzheimer’s disease (**LOAD**) risk alleles without relying on transgenic overexpression models. - Mice were followed longitudinally with regular behavioral measures and biometric sampling out to 24 months; blood and brain tissue were collected for transcriptomics, proteomics, human disease correlation, and neuropathology. - LOAD2.Mthfr677C>T mice did not develop hallmark pathologies such as amyloid plaque deposition or marked neuroinflammation when compared to LOAD2 controls. - Despite lack of classical amyloid pathology, LOAD2.Mthfr677C>T brains exhibited transcriptional and proteomic alterations related to the **cerebrovasculature**, **myelination**, and **synaptic biology**. - These molecular signatures in the mouse model recapitulated features observed in human LOAD patients, supporting the model’s relevance for studying non-amyloid aspects of ADRD. - The authors conclude that LOAD2.Mthfr677C>T is useful for investigating cerebrovascular compromise and other prodromal disease processes in late‑onset Alzheimer’s disease. - The study is a preprint and has not been peer-reviewed; funding was declared from the NIH Common Fund U54 AG054345. No competing interests were declared.
## Clinical Analysis & Structured Key Points
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Kevin P Kotredes 1 The Jackson Laboratory; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Kevin%2BP%2BKotredes%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kotredes%20KP&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AKevin%2BP%2BKotredes%2B) * [ORCID record for Kevin P Kotredes](http://orcid.org/0000-0001-7874-4139 "Open in new tab") * For correspondence: kevin.kotredes@jax.org Ravi S Pandey 2 JACKSON LABORATORY; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ravi%2BS%2BPandey%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Pandey%20RS&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ARavi%2BS%2BPandey%2B) * [ORCID record for Ravi S Pandey](http://orcid.org/0000-0001-9567-2851 "Open in new tab") Alaina M Reagan 1 The Jackson Laboratory; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Alaina%2BM%2BReagan%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Reagan%20AM&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAlaina%2BM%2BReagan%2B) * [ORCID record for Alaina M Reagan](http://orcid.org/0000-0001-9666-0879 "Open in new tab") Zeynep Sarica 3 Indiana University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Zeynep%2BSarica%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Sarica%20Z&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AZeynep%2BSarica%2B) Rita O'Rourke 1 The Jackson Laboratory; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gareth%2BR%2BHowell%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Howell%20GR&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGareth%2BR%2BHowell%2B) * [ORCID record for Gareth R Howell](http://orcid.org/0000-0003-0565-6474 "Open in new tab") * [Abstract](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5739153/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5739153/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5739153/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5739153/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.08.25.746973v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5739153/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Background: Late-onset Alzheimer's disease (LOAD) comprises more than 95% of all AD cases. Transgenic, overexpression animal models have off target side effects, do not effectively produce the heterogeneity observed clinically in LOAD patients, and are therefore not best suited for preclinical therapeutic development. The Model Organism Development and Evaluation for Late-onset Alzheimer's Disease (MODEL-AD) Consortium was established to develop novel mouse strains to model human-relevant genetic and environmental risk factors for LOAD. Methylenetetrahydrofolate reductase (MTHFR) is an enzyme in the folate/methionine pathway. Variants in the MTHFR gene, notably 677C>T, are associated with ADRD, and we have previously shown the Mthfr677C>T mouse model phenocopies humans carrying the variant and develop cerebrovascular deficits. Methods: To examine the contributions of Mthfr677C>T in the context of late-onset Alzheimer's disease (LOAD), MODEL-AD created a novel mouse strain on the C57BL/6J (B6) background that was homozygous for Mthfr677C>T, in combination with humanized Abeta;, APOEe4, and Trem2*R47H (referred to as LOAD2.Mthfr677C>T). Mice were assessed over multiple ages for disease-relevant phenotypes. Regular behavior measurements and biometric samples were collected longitudinally to 24 months of age. Blood and brain tissue were collected for transcriptomics, proteomics, human disease correlation, and neuropathology. Results: Despite lacking hallmark pathologies such as amyloid deposition and significant neuroinflammation, compared to LOAD2 controls, LOAD2.Mthfr677C>T mice showed transcriptional and proteomic signatures in the brain that relate to the cerebrovasculature, myelination, and synaptic biology, similar to those seen in human LOAD patients. Conclusions: These data further support the use of the LOAD2.Mthfr677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared NIH Common Fund, https://ror.org/001d55x84, U54 AG054345 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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