Debbie Guerrero-Given

TL;DR: It is found that pα-syn* is a major neurotoxic species inducing mitochondrial damage, fission, and mitophagy, therefore constituting a central player in PD pathogenesis and implicating p α- syn* as a key neurotoxic α-syn species and a therapeutic target.

TL;DR: Eliminating α2δ4 in mice abolishes rod synaptogenesis and synaptic transmission to rod ON-bipolar cells, and disrupts postsynaptic mGluR6 clustering, and offers insights into retinal pathologies associated with α2 δ4 dysfunction.

TL;DR: Three distinct roles are identified for CAST/ELKS as positive regulators of CaV2.1 channel density and it is suggested that they regulate release probability through a post-priming step that controls synaptic vesicle fusogenicity.

TL;DR: It is suggested that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype, and these biofilms may protect surviving bacteria from subsequent antibiotic challenges, and acts as a reservoir of viable bacteria once antibiotic exposure has ended.

TL;DR: It is proposed that CaV2.1 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing CaV1 levels to regulate neuronal circuit output.