Single-cell study links mitochondrial DNA damage and PINK1 response in Parkinson’s brainstem neurons
Published in Brain/Neurology, Diseases!, Journals.
Publication date: October 12, 2026.
A study published online in Brain on October 7 examines mitochondrial DNA in individual acetylcholine-producing neurons from the pedunculopontine nucleus, a brainstem region affected by Parkinson’s disease. University of Birmingham and Newcastle University researchers compared post-mortem Parkinson’s tissue with neurologically normal control tissue.
Sequencing revealed extensive large deletions in mitochondrial DNA, mainly in the “major arc,” which contains genes involved in cellular energy production. Most deletions exceeded 1,000 base pairs. The investigators also detected increased expression of PINK1, a mitochondrial quality-control regulator, particularly in samples from people who had survived longer after diagnosis.
The authors interpret the PINK1 response as a possible compensatory mechanism. This extends research beyond the dopamine-producing neurons usually associated with Parkinson’s and identifies mitochondrial maintenance as a direction for further investigation.
Evidence limits: These are observations in donated tissue, supported by molecular analyses and modelling. They do not establish that increasing PINK1 prolongs survival or that a treatment targeting this pathway benefits patients.
Sources: University of Birmingham announcement, October 7, 2026; Lu et al., Brain, DOI: 10.1093/brain/awag348.