Pegging Pathology on Mitochondrial Dysfunction Studies
strengthen suspicions about brain-disorder pathophysiology
By A. Nicola Schweitzer
The mitochondrion, powerhouse of the eukaryotic cell, sits
at the center of converging lines of brain-disorder
research. Researchers have implicated the organelle in the
pathophysiology of distinct conditions such as schizophrenia
and bipolar disorder. The motif of convergence extends to
results obtained by disparate approaches ranging from
molecular and biochemical to clinical, and from empirical to
hypothetical. In the brain, energy produced through
oxidative phosphorylation in the mitochondrion not only
sustains the excitability of the neurons, but also controls
intracellular calcium concentration that in turn regulates
synaptic transmission, signal transduction, and cellular
resilience.
Indications of metabolic-enzyme abnormalities in subjects
with brain disorders date back at least to the 1960s for
schizophrenia, says Frank Middleton, at the State University
of New York Upstate Medical University, who has contributed
to this literature. In 2000, Tadafumi Kato, currently at the
RIKEN Brain Science Institute in Tokyo, proposed that
mitochondrial dysregulation and consequent effects on energy
metabolism and calcium uptake could comprehensively account
for the pathophysiology of bipolar disorder.1 But progress
in the field has been limited by technological constraints.
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Posted by Robert Karl Stonjek.