Early Biomarkers of Alzheimer’s Disease
Session Number
Project ID: MEDH 09
Advisor(s)
Dr. Suraj Cherian; Northwestern University Feinberg School of Medicine
Discipline
Medical and Health Sciences
Start Date
22-4-2020 8:50 AM
End Date
22-4-2020 9:05 AM
Abstract
Alzheimer’s disease (AD) is an irreversible, progressive brain disorder characterized by the deterioration of memory, visuospatial ability, and executive function. Because this neurodegeneration happens slowly, early diagnosis and intervention is needed. This study utilizes a preclinical transgenic mouse model of AD, 5XFAD, because it is characterized by an increase in amyloid-β oligomers (AβOs) in the hippocampus. Preliminary results show that the excitability of CA1, primary output neurons in the hippocampus, are only altered in younger mice but not in older animals. Additional evidence shows an increase in levels of two cytokines in the hippocampus in the younger age group. These results point to a potential link between excitability of these neurons and neuroinflammation. The innate or adaptive systems characterized by alterations in microglia, astrocytes of the brain, and peripheral immune cells such as T cells may underlie the mechanism for the shift in excitability of the neurons. Because functional changes in neurons are typically accompanied by changes in morphology, hippocampal tissues (post recording of electrical activity) were fixed and stained to be imaged. Current efforts include 3D reconstruction of traced neurons and Sholl analysis to determine if morphology is altered in 5XFAD and their control wild type littermates across different age groups.
Early Biomarkers of Alzheimer’s Disease
Alzheimer’s disease (AD) is an irreversible, progressive brain disorder characterized by the deterioration of memory, visuospatial ability, and executive function. Because this neurodegeneration happens slowly, early diagnosis and intervention is needed. This study utilizes a preclinical transgenic mouse model of AD, 5XFAD, because it is characterized by an increase in amyloid-β oligomers (AβOs) in the hippocampus. Preliminary results show that the excitability of CA1, primary output neurons in the hippocampus, are only altered in younger mice but not in older animals. Additional evidence shows an increase in levels of two cytokines in the hippocampus in the younger age group. These results point to a potential link between excitability of these neurons and neuroinflammation. The innate or adaptive systems characterized by alterations in microglia, astrocytes of the brain, and peripheral immune cells such as T cells may underlie the mechanism for the shift in excitability of the neurons. Because functional changes in neurons are typically accompanied by changes in morphology, hippocampal tissues (post recording of electrical activity) were fixed and stained to be imaged. Current efforts include 3D reconstruction of traced neurons and Sholl analysis to determine if morphology is altered in 5XFAD and their control wild type littermates across different age groups.