ArticleMolecular neurobiology2017
TREM2 Overexpression has No Improvement on Neuropathology and Cognitive Impairment in Aging APPswe/PS1dE9 Mice.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Gain-of-function Modulation of TREM2 and its Impact on Amyloid-β and Tau Pathologies in Alzheimer's Disease: A Systematic Review and Meta-analysis of Animal Studies.Molecular neurobiology · 2026Pooled it
- Cholecalciferol (vitamin D3) is an agonist of the Alzheimer's disease-associated immune receptor TREM2.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Knockdown ofJournal of inflammation research · 2024Article
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- Potential role of TREM2 in high cholesterol‑induced cell injury and metabolic dysfunction in SH‑SY5Y cells.Experimental and therapeutic medicine · 2023Article
- Brain glucose metabolism and nigrostriatal degeneration in isolated rapid eye movement sleep behaviour disorder.Brain communications · 2023Article
- Dynamic insights into the effects of nonsynonymous polymorphisms (nsSNPs) on loss of TREM2 function.Scientific reports · 2022Article
- Hydroxysafflor Yellow A Inhibits AβNeurochemical research · 2022Article
- Protective effect of quercetin against the metabolic dysfunction of glucose and lipids and its associated learning and memory impairments in NAFLD rats.Lipids in health and disease · 2021Article
- Reduced TREM2 activation in microglia of patients with Alzheimer's disease.FEBS open bio · 2021Article
- Established Beta Amyloid Pathology Is Unaffected by TREM2 Elevation in Reactive Microglia in an Alzheimer's Disease Mouse Model.Molecules (Basel, Switzerland) · 2021Article
- Alzheimer's Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia.International journal of molecular sciences · 2021Review
- Review
- Danger-Sensing/Patten Recognition Receptors and Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Mechanistic insights into the deleterious roles of Nasu-Hakola disease associated TREM2 variants.Scientific reports · 2020Article
- Curcumin restores innate immune Alzheimer's disease risk gene expression to ameliorate Alzheimer pathogenesis.Neurobiology of disease · 2019Article
- Quercetin Alleviates LPS-Induced Depression-Like Behavior in RatsFrontiers in pharmacology · 2019Article
- Early compensatory responses against neuronal injury: A new therapeutic window of opportunity for Alzheimer's Disease?CNS neuroscience & therapeutics · 2019Review
- Triggering receptor expressed on myeloid cells 2 (TREM2): a potential therapeutic target for Alzheimer disease?Expert opinion on therapeutic targets · 2018Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we showed that overexpression of triggering receptor expressed on myeloid cells 2 (TREM2), a microglia-specific immune receptor, in the brain of a middle-aged (7 months old) APPswe/PS1dE9 mice could ameliorate Alzheimer's disease (AD)-related neuropathology by enhancement of microglial amyloid-β (Aβ) phagocytosis. Since AD is an age-related neurodegenerative disorder, it is critical to assess the efficacy of TREM2 overexpression in aging animals with an advanced disease stage. In vivo, we employed a lentiviral strategy to overexpress TREM2 in the brain of aging (18 months old) APPswe/PS1dE9 mice, and observed its efficacy on AD-related neuropathology and cognitive functions. Afterwards, we directly isolated microglia from middle-aged and aging APPswe/PS1dE9 mice and determined effects of TREM2 overexpression on microglial Aβ phagocytosis and Aβ-binding receptors expression in vitro. In aging APPswe/PS1dE9 mice, TREM2 overexpression has no beneficial effect on AD-related neuropathology and spatial cognitive functions. Of note, in vitro experiments showed a significant reduction of Aβ phagocytosis in microglia from aging APPswe/PS1dE9 mice, possibly attributing to the declined expression of Aβ-binding receptors. Meanwhile, this phagocytic deficit in microglia from aging APPswe/PS1dE9 mice cannot be rescued by TREM2 overexpression. Taken together, our study shows that TREM2 overexpression fails to provide neuroprotection in aging APPswe/PS1dE9 mice, possibly attributing to deficits in microglial Aβ phagocytosis at the late-stage of disease progression. These findings indicate that TREM2-mediated protection in AD is at least partially dependent on the reservation of microglial phagocytic functions, emphasizing the importance of early therapeutic interventions for this devastating disease.
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