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Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy
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Attention deficit-hyperactivity disorder suffers from mitochondrial dysfunction.

Poonam Verma1, Alpana Singh1, Dominic Ngima Nthenge-Ngumbau1

  • 1CSIR-Indian Institute of Chemical Biology, Laboratory of Clinical & Experimental Neurosciences, Cell Biology & Physiology Division, 4, Raja S.C. Mullick Road, Kolkata - 700032, India.

BBA Clinical
|November 30, 2016
PubMed
Summary

Mitochondrial defects are implicated in attention-deficit hyperactivity disorder (ADHD). This study found impaired cellular respiration and energy production in ADHD cybrids, suggesting a role for mitochondrial dysfunction in ADHD.

Keywords:
ATPaseCybridsMitochondrial membrane potentialMitochondrial pathologyRespirationSerotonin

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • The underlying pathophysiology of attention-deficit hyperactivity disorder (ADHD) remains largely unknown.
  • Mitochondrial dysfunction is increasingly recognized as a potential factor in various neurological disorders.

Purpose of the Study:

  • To investigate potential mitochondrial defects in cybrid cell lines derived from individuals with ADHD and control populations.
  • To explore the role of mitochondrial pathology in the development and presentation of ADHD.

Main Methods:

  • Cybrid cell lines were generated by fusing platelets from ADHD patients and controls with ρ0-cells.
  • Assessed cellular respiration, oxidative stress, mitochondrial membrane potential, and morphology using techniques like oxygraphy and FACS.
  • Quantified serotonin levels, mitochondrial ATPase 6/8 subunits, and complex V activity via HPLC, RT-PCR, and Blue Native PAGE.

Main Results:

  • ADHD cybrids exhibited significantly reduced cellular and mitochondrial respiration, lower ATPase6/8 transcript levels, and diminished mitochondrial complex V activity.
  • Observed a loss of mitochondrial membrane potential and elevated oxidative stress in ADHD cybrids.
  • Serotonin levels were increased in differentiated ADHD cybrid-neurons, while MAO-A and MAO-B levels were unaffected.

Conclusions:

  • The observed mitochondrial defects in ADHD cybrids, which replicate findings from post-mortem brains, strongly suggest mitochondrial pathology contributes to ADHD.
  • A bioenergetic crisis in mitochondria may be a significant factor in ADHD pathology and/or phenotypes.