Neurodevelopmental Disorders: Functional Role of Ambra1 in Autism and Schizophrenia

Livia La Barbera, Francescangelo Vedele, Annalisa Nobili, Marcello D’Amelio, Paraskevi Krashia

Research output: Contribution to journalReview article

Abstract

The activating molecule in Beclin-1-regulated autophagy (Ambra1) is a highly intrinsically disordered protein best known for its role as a mediator in autophagy, by favoring the formation of autophagosomes. Additional studies have revealed that Ambra1 is able to coordinate cell responses to stress conditions such as starvation, and it actively participates in cell proliferation, cytoskeletal modification, apoptosis, mitochondria removal, and cell cycle downregulation. All these functions highlight the importance of Ambra1 in crucial physiological events, including metabolism, cell death, and cell division. Importantly, Ambra1 is also crucial for proper embryonic development, and its complete absence in knock-out animal models leads to severe brain morphology defects. In line with this, it has recently been implicated in neurodevelopmental disorders affecting humans, particularly autism spectrum disorders and schizophrenia. Here, we discuss the recent links between Ambra1 and neurodevelopment, particularly focusing on its role during the maturation of hippocampal parvalbumin interneurons and its importance for maintaining a proper excitation/inhibition balance in the brain.

Original languageEnglish
Pages (from-to)6716-6724
Number of pages9
JournalMolecular Neurobiology
Volume56
Issue number10
DOIs
Publication statusPublished - Oct 1 2019

Keywords

  • Ambra1
  • Autism spectrum disorder
  • Autophagy
  • Excitation/inhibition
  • Hippocampus
  • Parvalbumin interneuron
  • Schizophrenia

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Neurology
  • Cellular and Molecular Neuroscience

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  • Cite this

    La Barbera, L., Vedele, F., Nobili, A., D’Amelio, M., & Krashia, P. (2019). Neurodevelopmental Disorders: Functional Role of Ambra1 in Autism and Schizophrenia. Molecular Neurobiology, 56(10), 6716-6724. https://doi.org/10.1007/s12035-019-1557-7