Yasir H. Qureshi

This study shows that disrupting SORL1-retromer recycling in mice leads to age-dependent brain atrophy resembling Alzheimer's disease, which can be reversed by restoring SORL1 function.

Pharmacological inhibition of RhoGEF12 increases endosomal SORL1-retromer recycling and reduces pathogenic amyloid secretion in human neuronal models, identifying a novel, targetable pathway for treating Alzheimer's disease.

The paper tests combinatorial gene therapy for retromer-related neurological diseases by expressing VPS35 with VPS26 paralogs in neurons, showing synergistic effects on retromer function and Sorl1 levels.

This study shows that restoring VPS35 in the hippocampus of mice with chronic neuronal VPS35 depletion rescues APP cleavage and glutamate receptor levels, and reduces glial activation similar to Alzheimer's disease.