Advisor(s)
Erik Roberson
Committee Member(s)
Jeremy Day
Jeremy Herskowitz
Karen Gamble
Lori McMahon
Rita Cowell
School
Joint Health Sciences (Interdisciplinary)
Document Type
Dissertation
Department (new version)
Neurobiology
Date of Award
9-11-2025
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disease and the leading cause of dementia. Genetics plays a large role in the risk of developing AD, with autosomal dominant mutations conferring almost 100% risk and sporadic mutations conferring a lower risk in a greater proportion of the population. Genome-wide association studies have helped to identify many genetic risk factors for AD, which can inform on various mechanisms of disease dysfunction. BIN1 is the second leading genetic risk factor for AD, after APOE. BIN1 has isoform-specific expression across cell types, which is differentially altered in AD brains. Here, we describe BIN1’s isoform- and cell-type-specific expression and explore the role of BIN1 in neurons. First, we examine BIN1’s role in parvalbumin-expressing neurons, which are altered in AD. We explore if and how a loss of Bin1 expression specifically from this neuron class can alter network activity. Next, we examine BIN1’s effect on L-type voltage-gated calcium channel (LVGCC) surface localization and calcium flux. Finally, we discuss the limitations, relevance, and future directions of our studies. Together, this work provides valuable insight into the neuronal role of BIN1, how it contributes to AD pathophysiology, and potential therapeutic avenues for AD detection and treatment.
ProQuest ID
Recommended Citation
Davis, Mary Natalie, "A Neuronal Role For Alzheimer’S Disease Risk Factor Bin1" (2025). All ETDs from UAB. 7354.
https://digitalcommons.library.uab.edu/etd-collection/7354
