Potential Mechanisms Driving Mitochondrial Motility Impairments in Developing Iron-Deficient Neurons

Research output: Contribution to journalComment/debatepeer-review

1 Scopus citations

Abstract

Brain development is highly demanding energetically, requiring neurons to have tightly regulated and highly dynamic metabolic machinery to achieve their ultimately complex cellular architecture. Mitochondria are the main source of neuronal adenosine 5′-triphosphate (ATP) and regulate critical neurodevelopmental processes including calcium signaling, iron homeostasis, oxidative stress, and apoptosis. Metabolic perturbations during critical neurodevelopmental windows impair neurological function not only acutely during the period of rapid growth/development, but also in adulthood long after the early-life insult has been rectified. Our laboratory uses iron deficiency (ID), the most common nutrient deficiency, as a model of early-life metabolic disruptions of neuronal metabolism because iron has a central role in mitochondrial function. Recently, we published that ID reduces hippocampal neuronal dendritic mitochondrial motility and size. In this commentary, we delve deeper into speculation about potential cellular mechanisms that drive the effects of neuronal ID on mitochondrial dynamics and quality control pathways. We propose that understanding the basic cellular biology of how mitochondria respond and adapt to ID and other metabolic perturbations during brain development may be a key factor in designing strategies to reduce the risk of later-life psychiatric, cognitive, and neurodegenerative disorders associated with early-life ID.

Original languageEnglish (US)
JournalJournal of Experimental Neuroscience
Volume13
DOIs
StatePublished - Jun 1 2019

Keywords

  • dendrite
  • development
  • energy metabolism
  • hippocampus
  • iron
  • mitochondria
  • neuron

PubMed: MeSH publication types

  • Journal Article
  • Comment

Fingerprint Dive into the research topics of 'Potential Mechanisms Driving Mitochondrial Motility Impairments in Developing Iron-Deficient Neurons'. Together they form a unique fingerprint.

Cite this