Presented By: Abid Hussaini, PhD
Speaker Biography: Dr. Abid Hussaini is an Assistant Professor in the Department of Pathology and Cell Biology at the Taub institute at Columbia University Irving Medical Center. He obtained his PhD in Neurobiology (2008) in Dr. Randolf Menzel’s laboratory at Freie Universitaet Berlin, Germany, studying sleep and olfactory memory. He completed his postdoctoral training (2014) in Dr. Eric Kandel’s laboratory at Columbia University, studying the role of HCN1 channels in spatial memory. His current research focuses on studying the regions of the brain most vulnerable to Alzheimer’s disease (AD). One of his major goals is to understand how amyloid beta and tau pathologies impact neuronal function in brain regions such as the entorhinal cortex – hippocampal circuit which is important for learning and memory. Using in vivo electrophysiology, optogenetics and chemogenetics techniques in mouse models of AD, his lab is beginning to identify neurons most affected by AD pathology. More recently, his lab also focuses on how AD affects locus coeruleus- a brain region involved in arousal and sleep. Apart from research, he is also contributing to open science initiatives such as Brainwiki.org.
Webinar: Understanding the Role of Alzheimer’s Disease Pathologies in Spatial Memory Dysfunction
Webinar Abstract: Some of the earliest symptoms of Alzheimer’s disease (AD) are loss of orientation, wandering and misplacing items. One of the first regions vulnerable to AD pathology is the entorhinal cortex (EC), and together with hippocampus (HPC), the EC-HPC circuit is intimately involved in several memory functions, including spatial memory. Using mouse models of Alzheimer’s disease, I will show how amyloid beta and tau pathologies affect neuronal and network function in the EC-HPC circuit. More specifically, I will show how the neural correlates of spatial memory, the place cell and the grid cells are impacted by AD pathologies. Further, I will demonstrate how neuronal activity influences pathology and if modulating the neuronal activity can rescue neurodegeneration.
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