Expression of microRNA-34a in Alzheimer’s disease brain targets genes linked to synaptic plasticity, energy metabolism, and resting state network activity
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MiR-34a/c promotes apoptosis and impairs synaptic plasticity; their inhibition rescues memory in AD mouse models.
“MiR-34a/c also promotes apoptosis and impair synaptic plasticity; their inhibition rescues memory in AD mouse models (Banzhaf-Strathmann et al., 2014; Sarkar et al., 2016; Zovoilis et al., 2011).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Sarkar et al., 2016
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 Sarkar et al., 2016
Through repression of TREM2 and SIRT1, miR-34a lowers microglial capacity to clear Aβ and promotes a sustained inflammatory phenotype, contributing to synaptic and metabolic decline.
“Through this repression, miR-34a lowers microglial capacity to clear Aβ and promotes a sustained inflammatory phenotype, contributing to synaptic and metabolic decline (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 Sarkar et al., 2016
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- Authors
- Sarkar, S., Jun, S., Rellick, S., Quintana, D. D., Cavendish, J. Z., & Simpkins, J. W.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2016-09
- Volume
- 1646
- Pages
- 139-151
- ISSN
- 0006-8993
- PMC
- PMC4975975
- Cited by
- 185
- References
- 10
- Language
- en
- Funders
- National Institutes of Health (P01 AG027956, PO1 AG022550)
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