ArticleActa neuropathologica communications2021
TREM2 modulates differential deposition of modified and non-modified Aβ species in extracellular plaques and intraneuronal deposits.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Remodeling of the brain immune microenvironment in Alzheimer's disease: interactions among microglia, astrocytes, complement, and the neurovascular unit.Frontiers in immunology · 2026Review
- Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Loss of TREM2 diminishes CAA despite an overall increase of amyloid load in Tg-SwDI mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Microglia and Astrocytes in Alzheimer's Disease: Significance and Summary of Recent Advances.Aging and disease · 2024Review
- Phosphorylation-state dependent intraneuronal sorting of Aβ differentially impairs autophagy and the endo-lysosomal system.Autophagy · 2024Article
- miR155, TREM2, INPP5D: Disease stage and cell type are essential considerations when targeting clinical interventions based on mouse models of Alzheimer's amyloidopathy.Journal of neuroinflammation · 2023Article
- Acute and Chronic Macrophage Differentiation Modulates TREM2 in a Personalized Alzheimer's Patient-Derived Assay.Cellular and molecular neurobiology · 2023Article
- Step by step: towards a better understanding of the genetic architecture of Alzheimer's disease.Molecular psychiatry · 2023Review
- APOE and immunity: Research highlights.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Matrix Development for the Detection of Phosphorylated Amyloid-β Peptides by MALDI-TOF-MS.Journal of the American Society for Mass Spectrometry · 2023Article
- Definition of the contribution of an Osteopontin-producing CD11cProceedings of the National Academy of Sciences of the United States of America · 2023Article
- TREM2 risk variants are associated with atypical Alzheimer's disease.Acta neuropathologica · 2022Article
- Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive accumulation of Amyloid-β (Aβ) deposits in the brain is a characteristic neuropathological hallmark of Alzheimer's disease (AD). During disease progression, extracellular Aβ plaques undergo specific changes in their composition by the sequential deposition of different modified Aβ species. Microglia are implicated in the restriction of amyloid deposits and play a major role in internalization and degradation of Aβ. Recent studies showed that rare variants of the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) are associated with an increased risk for AD. Post-translational modifications of Aβ could modulate the interaction with TREM2, and the uptake by microglia. Here, we demonstrate that genetic deletion of TREM2 or expression of a disease associated TREM2 variant in mice lead to differential accumulation of modified and non-modified Aβ species in extracellular plaques and intraneuronal deposits. Human brains with rare TREM2 AD risk variants also showed altered deposition of modified Aβ species in the different brain lesions as compared to cases with the common variant of TREM2. These findings indicate that TREM2 plays a critical role in the development and the composition of Aβ deposits, not only in extracellular plaques, but also intraneuronally, that both could contribute to the pathogenesis of AD.
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