Join us virtually for the 3rd Annual Cognitive Neuroscience of Development and Aging (CoNDA) Center Colloquium! We will hear presentations from current and upcoming CoNDA-funded investigators, and the event will conclude with a keynote seminar from Dr. David M. Holtzman of Washington University in St. Louis. Please see below for the full Colloquium schedule and more details on Dr. Holtzman's talk.

9:15 – 9:20am: Welcome: Dr. Anna Dunaevsky – CoNDA Center Director

9:20 – 9:45am: Research Project Leader: Dr. Leo Augusto – UNMC |  The Role of Host Amino Acid Metabolism in Behavioral Changes during Latent Toxoplasmosis

9:45 – 10:05am: Pilot Project: Dr. Valentina Gumenyuk – UNMC | Brain Biomarkers for Early Detection of Neurodegeneration in Temporal and Frontal areas in patients with FTD, LDB, and AD: EEG/MEG Study

10:05 – 10:15am: New Pilot Project: Dr. Yutong Liu – UNMC | CEST MRI for Neuropathology of ART and Nicotine

10:15 – 10:25am: CoNDA Mini-Grant Recipient: Jennifer Sexton | Neurodevelopmental Effects of Polygenic AD Risk in Children with Down Syndrome

10:25 – 10:35am: Break

10:35 – 10:55am: Pilot Project: Dr. Jee-Yeon Hwang – Creighton University | Neuroinflammation in Neurodegeneration and Cognitive Impairment Associated with Global Ischemia

10:55 – 11:05am: New Pilot Project: Dr. Vijaya Bhatt – UNMC | Neural Basis of Cognitive Impairments in Older Adults with Myeloid Malignancies

11:05 – 11:30am: New Research Project: Dr. Peng Zhong – UNMC | Dysfunction of Lateral Hypothalamic Sleep Neurons in Alzheimer’s Disease

11:30 – 11:55am: Research Project Leader: Dr. Olga Taraschenko – UNMC | The Role of Hippocampal Neurogenesis in the Development of in Autoimmune Encephalitis with Seizures

11:55am – 12:00pm: Break

12:00 – 1:00pm: Keynote: Dr. David Holtzman – Washington University | Role of APOE in Tau-mediated Neurodegeneration: Effects on Microglial Lipid Metabolism and the Immune Response

• ABSTRACT: Apolipoprotein E (APOE) genotype is a major risk factor for Alzheimer’s disease (AD).  The effect of APOE on amyloid deposition likely accounts for a major part of the increased risk for AD. Recent studies in mouse models and in humans also suggest that APOE plays an important role in tau-mediated neurodegeneration.  For example, in a mouse model of tauopathy, P301S Tau transgenic mice, we have found that human APOE isoforms contribute to tau-mediated neurodegeneration in the order E4>E3>E2.  Further, the absence of APOE is highly neuroprotective in this model and specific removal of APOE4 from astrocytes is also very protective.  Removal of microglia in the P301S mice is similarly neuroprotective as the complete removal of APOE.  In recent studies, we have found that in the P301S model, as neurodegeneration develops, there is a very strong accumulation of neutral lipids in microglial lysosomes and this occurs to a much greater extent in the presence of APOE4 than with either APOE3 or murine ApoE.  APOE, in particular APOE4 may be contributing to tau-mediated neurodegeneration via impairing microglial lipid trafficking. In addition to these findings, new insights into the potential role of the innate and adaptive immune response in tauopathy will also be presented.