Garth J. S. Cooper

TL;DR: It is demonstrated that postmortem human brain urea levels are elevated in a larger cohort of HD cases, including those with low-level neuropathology (Vonsattel grade 0/1), which indicates increased protein catabolism, possibly as an alternate energy source given the generalized metabolic defect in HD.

TL;DR: It is proposed that diabetes-evoked copper dysregulation is an important new target for therapeutic intervention to prevent/reverse organ damage in diabetes, heart failure, and neurodegenerative diseases, and that triethylenetetramine (TETA) is the first in a new class of anti-diabetic molecules, which function by targetting these copper-mediated pathogenic mechanisms.

TL;DR: This study strengthens the view that human amylin kills pancreatic islet β‐cells by apoptosis, and demonstrates that electron microscopy is a more sensitive tool for early apoptosis detection in cultured cells than classical biochemical assays like visualizing DNA laddering.

TL;DR: Elevation of brain glucose and deficient brain copper potentially contribute to the pathogenesis of neurodegeneration in AD.

TL;DR: It is reported that amylin caused a dose‐dependent increase in activity of muscle glycogen phosphorylase in isolated rat soleus muscle by stimulating phosphory lase a, which could be a major mechanism whereby amyl in modulates carbohydrate metabolism.