Topic: mitochondrial damage

The kinase-ligase pair PINK1-PRKN recognizes and selectively labels worn-out and dysfunctional mitochondria with phosphorylated ubiquitin (pS65-Ub) to facilitate their elimination via autophagy (mitophagy). Although typically transient, pS65-Ub serves as a quantitative marker of mitochondrial damage but can also remain elevated due to insufficient degradation and flux through lysosomes. In human autopsy brain, the number of pS65-Ub positive cells increases with age but is also independently associated with Lewy body (LB), neurofibrillary tangles (NFT), and senile plaque (SP) burden. However, p

Heat shock protein 60 (Hsp60) functions as a molecular chaperone, playing a vital role in maintaining protein homeostasis by regulating protein folding and preventing protein aggregation. Levels of heat shock proteins increase in response to oxidative stress and mitochondrial damage, both of which are symptoms commonly associated with various forms of epilepsy. Hsp60 levels are increased in the plasma of patients with temporal lobe epilepsy (TLE). It is crucial to understand what conformations and functions Hsp60 obtains within its folding cycle to determine Hsp60’s role in seizure response. F