Dysregulation of astrocyte–neuronal communication in Alzheimer’s disease

Carmen Nanclares, Andres Mateo Baraibar, Alfonso Araque, Paulo Kofuji

Research output: Contribution to journalReview articlepeer-review

Abstract

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.

Original languageEnglish (US)
Article number7887
JournalInternational journal of molecular sciences
Volume22
Issue number15
DOIs
StatePublished - Jul 23 2021

Bibliographical note

Funding Information:
This work was supported by the National Institutes of Health-NINDS (R01NS097312), National Institutes of Health-NIDA (R01DA048822), National Institutes of Health-NIMH (R01MH119355), and Postdoctoral Research Fellowship from the Basque Government (POS_2019_0041).The authors would like to thank Dana Deters for expert laboratory assistance. view Board Statement: Not applicable. Figures created in Biorender, https://biorender.com, 9 June 2021.

Funding Information:
editedandfinalizetdionthael ImnsatintutsecsroifpHt.eAalltlha-NuItDhoAr(sRh0a1vDeA r0e4a8d82a2n),dNatgioreneadlIntostitthuet epsuofbHlisehaletdh-NveIMrsHion(Ro01f MH119355), the manuscript. and Postdoctoral Research Fellowship from the Basque Government (POS_2019_0041).

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Alzheimer’s disease
  • Amyloid plaques
  • Calcium
  • Glia
  • Gliotransmission

PubMed: MeSH publication types

  • Journal Article
  • Review

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