Jorge Palop’s lab aims to understand the neural processes underlying cognitive decline in Alzheimer’s disease and neurological conditions, such as epilepsy, autism, and schizophrenia. His team focuses on a type of neuron that stabilizes neuronal networks in the brain, called inhibitory interneurons, and the role they may play in the cognitive dysfunction and abnormal patterns of neuronal network activity that accompany Alzheimer’s disease. Ultimately, Palop’s group aims to define the mechanisms of cognitive dysfunction at the molecular, circuit, and network level, as well as to develop novel therapeutic approaches to restore brain functions in Alzheimer’s disease.
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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.
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