Topic: mitochondrial DNA

Investigate mitochondrial DNA architecture and function at LNBio/CNPEM in Campinas with Thayna Mendonça Avelino. Combine coherent X-ray diffraction imaging with STED microscopy, develop multimodal imaging strategies and integrate structural and functional measurements. The fellowship starts in November 2026. Submit a CV, motivation letter and recommendation letter to the investigator’s address on the official call by 12 October 2026.

One of the primary pathological factors implicated in Alzheimer's disease (AD) is the beta-amyloid peptide (Aβ), known for its various toxic effects including decreased cytosolic ATP levels and elevated intracellular calcium. Our laboratory's research has revealed that Aβ treatments induce alterations in mitochondrial morphology and dynamics in animal models of AD, leading to increased ROS generation and potential leakage of mitochondrial elements like mitochondrial DNA (mtDNA) into the cytoplasm. MtDNA can activate the inflammatory response via cyclic GMP-AMP synthase (cGAS), triggering proin

In Parkinson’s disease (PD), patients often exhibit higher levels of somatic mitochondrial DNA (mtDNA) damage, particularly large-scale deletions, in their brains. This damage is associated with losing neurons, including nigral dopaminergic and cholinergic neurons in the Pedunculopontine Nucleus (PPN). Unlike dopaminergic neurons, PPN cholinergic neurons tend to maintain wild-type mtDNA levels by increasing mtDNA copy number (mtCN) in response to mtDNA deletions.Our study isolated single cholinergic neurons from post-mortem PPN tissue of PD patients and controls, examining mtDNA deletions' loc