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Knight Initiative for Brain Resilience Monthly Seminar

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The first Monday of each month, the Knight Initiative for Brain Resilience will host monthly seminars to bring together awardees, affiliated professors and students for a series of 'lab meeting' styled talks. Two speakers will discuss their brain resilience research, experiences in the field, and answer questions about their work.

Congcong Wang, Stanford University

Peripheral prostaglandin E2 signaling inhibition restores cognitive decline in aging

Aging is characterized by the development of maladaptive pro-inflammatory responses in both the periphery and brain. Emerging studies demonstrate that circulatory age-related factors can modulate brain cognitive decline. However, the underlying mechanisms are not well defined. En route to the highly vascularized and energy-demanding brain, circulating factors first reach the blood-brain barrier (BBB), which mainly consists of brain endothelial cells (BECs). Here we find that pharmacologic inhibition of peripheral prostaglandin E2 (EP2) receptor, a dominant modulator of inflammation, prevents age-dependent myeloid-biased blood composition, systemic and brain pro-inflammatory states, and hippocampal memory decline. In aging BBB, peripheral EP2 inhibition rejuvenates the aging BECs transcriptome and cerebrovascular integrity. In the brain, peripheral EP2 inhibition rescues age-associated energy-deficient state, including tricarboxylic acid (TCA) cycle pathways and lactate production, suggesting youthful neuronal bioenergetics. Our study suggests that targeting peripheral EP2 signals is sufficient to restore cerebrovascular and cognitive decline in aging. 

Patrick Purdon, Harvard University

Dynamic Disruption: A Fundamental Mechanism of Anesthesia and A Window into Brain Resilience

How do anesthetic drugs produce states of unconsciousness? Although the answer to this question is widely regarded to be a mystery, a growing body of evidence suggests that that anesthetic drugs produce different states of unconsciousness in part by inducing profound neurophysiologic oscillations that disrupt different aspects of brain function. The form of these oscillations appears to relate directly to the underlying molecular- and circuit-level neuropharmacology for these drugs, such that each anesthetic drug class has a unique “EEG signature.” Many patients who undergo surgery under general anesthesia, particularly those who are older or who have pre-existing cognitive impairment, develop post-operative neurocognitive disorders such as delirium or cognitive dysfunction. There is evidence that a substantial fraction of these poor neurocognitive outcomes are attributable to anesthetic exposure, and that these outcomes are related to features of the patient’s anesthesia-induced EEG. In this presentation we will 1) examine the neurophysiological mechanisms of anesthetic drugs, 2) review emerging evidence relating anesthesia-induced brain oscillations to brain resilience and risk for post-operative neurocognitive disorders, and 3) briefly examine new neural signal processing tools developed by the PurdonLab that could be used to characterize and track brain resilience and cognitive decline with far greater accuracy and precision than existing methods.

Patrick Purdon will be joining Stanford University School of Medicine as a Professor of Anesthesiology later this year. He is currently an Associate Professor of Anaesthesia at Harvard Medical School and the Nathaniel M. Sims Endowed Chair in Anesthesia Innovation and Bioengineering at Massachusetts General Hospital. Patrick Purdon received his A.B. in Engineering Sciences from Harvard College in 1996, his M.S. in Electrical Engineering from MIT in 1998, and his Ph.D. in Biomedical Engineering from MIT in 2005. Patrick Purdon’s research focuses on the mechanisms of anesthesia and post-operative neurocognitive disorders, neural signal processing, and the EEG/MEG inverse problem.

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