Cited by 185

Expression of microRNA-34a in Alzheimer’s disease brain targets genes linked to synaptic plasticity, energy metabolism, and resting state network activity

Sarkar, S., Jun, S., Rellick, S., Quintana, D.D., Cavendish, J.Z., Simpkins, J.W.·2016·Brain Research

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Crossref · 10.1016/j.brainres.2016.05.026

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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).”
  • 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).”
  • 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).”

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Research works printed but not linked: 43

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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
Cited by
185
References
10
Language
en
Funders
National Institutes of Health (P01 AG027956, PO1 AG022550)

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