Jorge Palop, PhD

Palop discovered that mice genetically engineered to simulate Alzheimer's disease (by producing excess beta-amyloid protein) develop aberrant patterns of neuronal network activity, including abnormal synchronisation and seizures. These patterns resemble the epileptic symptoms observed in many patients with early-onset familial Alzheimer’s disease, the hyperactivation of neuronal networks detected in patients with sporadic Alzheimer’s disease, and in non-demented people who carry amyloid deposits.

Palop and his team found that in Alzheimer’s mouse models, these symptoms could be attributed to the alteration of inhibitory interneurons. Importantly, they showed that by supplying genetically modified interneurons in the brain of Alzheimer’s mice, or by chemically enhancing the function of resident interneurons, they could restore the cognitive functions and brain oscillatory rhythms in these mice. The findings pave the way for therapeutic interventions targeting the function of inhibitory interneurons, which the lab is currently pursuing through a combination of cell-based and pharmacological approaches.