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Deficits in the miRNA-34a-regulated endogenous TREM2 phagocytosis sensor-receptor in Alzheimer’s disease (AD); an update

Bhattacharjee, Surjyadipta, Zhao, Yuhai, Lukiw, Walter J.·2014·Frontiers in Aging Neuroscience
DOI 10.3389/fnagi.2014.00116PMC PMC4060025
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  • MiR-34a is strongly induced in AD and directly represses TREM2 and SIRT1, both essential for microglial metabolic fitness, phagocytosis, and transition into the disease-associated microglial (DAM) state.

    “MiR-34a is also strongly induced in AD and exerts multifaceted pathogenic effects. It directly represses TREM2 and SIRT1, both essential for microglial metabolic fitness, phagocytosis, and transition into the disease-associated microglial (DAM) state (Bhattacharjee et al., 2014; Sarkar et al., 2016; Sarkar et al., 2019).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Bhattacharjee et al., 2014

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Authors
Bhattacharjee, S., Zhao, Y., & Lukiw, W. J.
Venue
Frontiers in Aging Neuroscience
Publisher
Frontiers Media SA
Published
2014-06-17
Volume
6
ISSN
1663-4365
DOI
10.3389/fnagi.2014.00116
PMC
PMC4060025
Cited by
24
References
6

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