[Life Sciences Seminar]
▶Subject: Neuronal hyperexcitation in HIV infection and Alzheimer’s disease
▶Speaker: Seonil Kim, Ph.D. (Department of Biomedical Sciences, Colorado State University)
▶Date: 4:00PM/Jan. 9(Thu.)/2020
▶Place: Room #104, Life Science Bldg.
Neuronal hyperexcitability is found in various brain disorders including HIV-associated neurocognitive disorders (HANDs) and Alzheimer’s disease (AD). However, underlying mechanisms have not been fully understood. Interestingly, feline immunodeficiency virus (FIV) naturally infects cats and shares its structure, cell tropism, and pathology with HIV, including wide-ranging neurological deficits. We employ FIV as a model to elucidate the molecular pathways underlying HIV-induced neuronal dysfunction, in particular, synaptic alteration. In particular, we have revealed viral glycoprotein-induced neuronal hyperexcitation requires aberrant neuronal cGMP-dependent protein kinase II (cGKII) activation. We further confirm that FIV and HIV share the cGKII-mediated core cellular pathway that induces neuronal dysfunction. Beta-amyloid (Aβ) peptide accumulation has long been implicated in the pathogenesis of AD. We find beta-amyloid peptide (Aβ) reduces the activity of hippocampal interneurons via selective inhibition of α7 and α4β2 nicotinic acetylcholine receptors (nAChRs), resulting in neuronal hyperexcitation in excitatory cells. Moreover, co-activation of α7 and α4β2 nAChRs is sufficient to abolish the Aβ effects on hippocampal inhibitory and excitatory neurons. Taken together, cellular mechanisms underlying neuronal hyperexcitation in both HANDs and AD can play crucial roles in both disease pathogenesis, thus strategies blocking neuronal hyperexcitation can be neuroprotective in both diseases.
▶Inquiry: Prof. Seung Tae Baek (279-2360)
* This seminar will be given in English.
Please refrain from taking photos during seminars. *