<i>A1527G</i> variant of ABCA7 increases soluble and insoluble Aβ40‐42 in an animal model for late‐onset Alzheimer's disease.
Data collected to date support a model whereby variations in ABCA7 exert risk for AD through interactions between cerebrovasculature, microglia, Aβ deposition, and peripheral immune cells.
Authors
- Kevin P. Kotredes (ORCID: https://orcid.org/0000-0001-7874-4139)
- G Carter
- Gareth R. Howell (ORCID: https://orcid.org/0000-0003-0565-6474)
- Michael Sasner (ORCID: https://orcid.org/0000-0002-6612-6111)
- Ravi S. Pandey (ORCID: https://orcid.org/0000-0001-9567-2851)
- Paul R. Territo (ORCID: https://orcid.org/0000-0003-0460-332X)
- Cristian Bernabe (ORCID: https://orcid.org/0000-0003-3466-0798)
- Bruce T Lamb
- Adrian L Oblak
Institutions
- Neurosciences Institute (US)
- Jackson Laboratory (US)
- Indiana University School of Medicine
- Indiana University – Purdue University Indianapolis (US)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1002/alz70860_103215
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00