Related Experiment Video
Updated: May 11, 2026
09:33
Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Cellular insights into transposable elements in Alzheimer's disease
Vikas Kumar1,2, Samuel Beck1
1Center for Aging Research, Department of Dermatology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA, United States.
Frontiers in Molecular Biosciences
|January 23, 2026
Summary
Transposable elements (TEs) are activated in Alzheimer's disease (AD), particularly in excitatory neurons and oligodendrocytes. This widespread TE dysregulation offers new avenues for understanding AD pathogenesis and developing therapies.
Area of Science:
- Genomics
- Neuroscience
- Molecular Biology
Background:
- Alzheimer's disease (AD) is a major neurodegenerative disorder with complex genetic underpinnings.
- Single-cell technologies have revealed cellular and transcriptional alterations in AD, but the role of transposable elements (TEs) is unclear.
Purpose of the Study:
- To investigate the cell type-specific landscape of TE expression and regulation in Alzheimer's disease.
- To identify specific TEs and their regulatory roles in AD pathogenesis.
Main Methods:
- Integration of single-nucleus RNA sequencing and ATAC-seq data from AD patients and controls.
- Mapping of cell type-specific TE expression and chromatin accessibility.
Main Results:
- Identification of 508 differentially expressed TE loci, with 84.3% upregulated in AD.
- Widespread TE activation observed, predominantly in excitatory neurons and oligodendrocytes.
- Dysregulated TEs found near key AD-associated genes (e.g., DOC2A, ABCA7, TARDBP).
Conclusions:
- TE activation is a significant feature of Alzheimer's disease, varying by cell type.
- TE dysregulation may contribute to AD pathogenesis through regulatory disruption.
- These findings provide a basis for exploring TEs as therapeutic targets in AD.
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