Mitochondrial dysfunction
Complex I deficits, PINK1/Parkin mitophagy and bioenergetic failure in dopaminergic neurons.
State of the art
No update yet for Mitochondrial dysfunction. An update is a standalone state-of-the-art for the topic — what someone with Parkinson's needs to know about where this approach stands today.
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Genome-wide association and population-tailored polygenic risk for Parkinson’s disease in Taiwan
A suggestive GWAS signal at PPARGC1A (rs609501; OR 1.22; P=3.5×10⁻⁶) — encoding PGC-1α, a master regulator of mitochondrial biogenesis — nominates this locus as a Taiwan-relevant PD risk factor, supported by prior rare-variant data in Han Chinese and epidemiological evidence linking the PPARγ agonist pioglitazone to lower PD incidence in Taiwan. -
Region-specific cortico-striatal transcriptomic remodeling following early postnatal dopaminergic disturbance
Gene co-expression network analysis identified two clusters negatively correlated with early dopaminergic disturbance: the "black" module (mitochondrial ATP synthesis, cellular respiration) and the "brown" module (tricarboxylic acid cycle, mitochondrial electron transport, ubiquitin-independent protein catabolism). A third cluster positively correlated with dopamine loss ("midnightblue") was linked to oxidative phosphorylation and reactive oxygen species responses, suggesting that dopamine loss triggers both a deficit and a compensatory stress response in mitochondrial gene programs within the corticostriatal circuit.