Michael T. Lin

TL;DR: Treatments targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria hold great promise in ageing-related neurodegenerative diseases.

TL;DR: It is demonstrated that primary neurons from Tg2576 mice recapitulate the in vivo localization and accumulation of Aβ42 with time in culture, and that A β42 aggregates into oligomers within endosomal vesicles and along microtubules of neuronal processes, which are associated with pathological alterations within processes and synaptic compartments in Tg 2576 mouse and human AD brains.

TL;DR: Blocking SK channels facilitates the induction of long-term potentiation by enhancing NMDAR-dependent Ca2+ signals within dendritic spines, mediated by a feedback loop within the spine head.

TL;DR: It is reported that cultured Tg2576 APP mutant neurons have selective alterations in pre- and post-synaptic compartments compared to wild-type neurons, and evidence is provided that Abeta is specifically involved in these alterations in synaptic biology.

TL;DR: It is found that brain mtDNA from elderly subjects had a higher aggregate burden of mutations than brain mt DNA from younger subjects, and Cytochrome oxidase activity correlated negatively with increasing mutational burden.