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Mitochondria modulate programmed neuritic retraction.

Sergei V Baranov1, Oxana V Baranova1, Svitlana Yablonska1

  • 1Neuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213.

Proceedings of the National Academy of Sciences of the United States of America
|December 26, 2018
PubMed
Summary
This summary is machine-generated.

Mitochondrial damage in neuronal processes, termed "neuritosis," impairs function and triggers non-lethal apoptosis. This process, exacerbated by aging and neurodegeneration, underlies synaptic vulnerability.

Keywords:
caspase-3mitochondrial membrane potentialmutant huntingtinneurite retractionneurodegeneration

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Neuritic retraction occurs in aging and neurodegenerative diseases without neuronal death.
  • Intracellular mechanisms driving neuritic retraction are poorly understood.

Purpose of the Study:

  • To investigate the role of distal mitochondrial damage in neuritic retraction.
  • To propose and validate a novel mechanism termed "neuritosis".

Main Methods:

  • Primary cerebrocortical neuron culture.
  • Mitochondrial protein damage assessment.
  • PINK1 accumulation and reactive oxygen species (ROS) measurement.
  • Mitochondrial membrane potential analysis.
  • In vivo mouse studies.

Main Results:

  • Mitochondrial damage, PINK1 accumulation, and ROS production increase with distance from the soma.
  • Distal mitochondria exhibit decreased membrane potential and depolarization threshold.
  • A distance-dependent mitochondrial membrane potential gradient was observed in vivo.
  • Impaired distal mitochondria show lower threshold for non-lethal caspase-3 activation.

Conclusions:

  • Cumulative distal mitochondrial damage leads to dysfunction and focal apoptosis in neurites (neuritosis).
  • This process contributes to synaptic vulnerability in normal aging, stress, and neurodegeneration.