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Please join us for PhD Student, Oghenetega Imiruaye give his PhD Literature Mastery Presentation.
Alzheimer’s disease (AD) is the most prevalent and persistent neurodegenerative condition. Beta-amyloid (Aβ) plaque deposition, accumulation of neurofibrillary tangles (NFTs), inflammation, dysregulated neurotransmitter signaling, brain atrophy, and neuronal alterations are the primary neuropathological hallmarks of AD. The central nervous system (CNS) is typically affected in AD, causing neuronal apoptosis, cognitive decline, memory loss, and death. Glutamate is the principal excitatory neurotransmitter in the CNS. Its action on ligand-gated ion channel receptors: NMDA and AMPA, regulate its uptake and recycling, which are critical in glutamatergic signaling and AD. NMDA receptors are ubiquitous in all brain areas, with the GluN2A and GluN2B-containing NMDARs localized in the hippocampal and cortical regions playing a significant role in AD pathogenesis by triggering excitotoxicity and neurodegeneration associated with AD. Recently, GluN2D receptors are also being investigated for their novel roles in AD. Ca2+ influx and total receptor blockade balance prevent excitotoxicity and neuronal dysfunction, ensuring proper neuronal function and plasticity. Activation of extrasynaptic NMDARs, NFTs, and uncontrolled glutamate secretion in the brain elicits excitotoxicity, damages the cells, and disrupts the blood-brain barrier integrity, ultimately relating to the progression of AD and complicating diagnosis and therapeutics.
Date: Tuesday, December 6, 2022
Time: 1:00 – 2:00 p.m.
Location: 535 Bldg. – 152 Classroom and Via Zoom (See Outlook invite for Zoom link)