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Student Seminars

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TBA

Yoland Smith, PhD - Division Chief, Neuropharmacology and Neurology Disease, Emory National Primate Research Center

 Jun 01, 2023 @ 4:00 p.m.

Host: John Foxe

TBA

Dean Salisbury, PhD - Director Clinical Neurophysiology Research Lab, Professor of Psychiatry, University of Pittsburgh

 May 18, 2023 @ 4:00 p.m.

Host: John Foxe

NSC 503 Seminars

Linh Le; Matt Adusei - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Brian Keane & Juliette McGregor

 May 01, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Alexis Feidler; Estephanie Balbuena - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Erika ANderson & Dragony Fu

 Apr 24, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Claire Lim; Tanique McDonald - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Margot Mayer-Proschel & Jean Bidlack

 Apr 17, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Andrea Campbell; Dominic Bunn - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Jude Mitchell & Gail Johnson

 Apr 10, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Daulton Myers; Margaux Masten - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Wei Hsu & David Dodell-Feder

 Apr 03, 2023 @ 4:00 p.m.

 Medical Center | K-307

Mary Notter Lectureship: TBA

Katalin Gothard, MD, PhD - Professor, Departments of Physiology and Neuroscience, University of Arizona

 Mar 30, 2023 @ 4:00 p.m.

Host: Lizabeth Romanski

NSC 503 Seminars

Erin Murray; Mariah Marrero - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Marissa Sobolewski & Suzanne Haber

 Mar 27, 2023 @ 4:00 p.m.

 Medical Center | K-307

Guest Speaker

 Mar 20, 2023 @ 4:00 p.m.

 Medical Center | Ryan Case Method Rm (1-9576)

Guest Speaker

 Mar 13, 2023 @ 4:00 p.m.

 Medical Center | Lower Adolph Aud. (1-7619)

NSC 503 Seminars

Abigail Alpers; Jeeyun Kim - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Ed Freedman & Marc Schieber

 Feb 27, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Lia Calcines Rodriguez - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Krishnan Padmanabhan & Martina Poletti

 Feb 20, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Julia Granato - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Ian Fiebelkorn & Greg DeAngelis

 Feb 13, 2023 @ 4:00 p.m.

 Medical Center | K-307

Determining the role of pericapillary spaces in the glymphatic system

Michael Giannetto - PhD Candidate, Advisor: Maiken Nedergaard, MD, DMSc

The brain is the most metabolically active organ in the body, yet it lacks a traditional lymphatic system for waste clearance. Instead, the brain utilizes the glymphatic system, a network of fluid filled spaces surrounding blood vessels, termed perivascular spaces (PVSs), which facilitates movement of cerebrospinal fluid (CSF) into the brain along arteries and waste clearance out of the brain along veins. Astrocytic endfeet comprise the outer boundary of the PVS and serve as a point of regulation for CSF flow into the brain. CSF flow in pial artery PVSs is well characterized to follow the same direction as blood flow driven by cardiac pulsations, and CSF flow is increased by large arterial dilations associated with neuronal activity. However, the function, and even existence, of the PVS along capillaries remains unclear. Additionally, the physiological function of pericytes, mural cells that cover capillaries, remains controversial. Some groups claim pericytes are important in blood flow regulation while others have demonstrated they are irrelevant to blood flow, but instead could maintain the extracellular matrix and phagocytose waste. Capillaries make up the bulk of vasculature surface area in the brain, with no brain tissue further than 30 micrometers away from a capillary, and capillaries are continuously covered by pericytes. Thus, capillary PVSs and pericytes are well positioned to clear waste but remain understudied. In this proposal, I will determine if there is directional fluid flow in capillary PVSs, test if pericytes contribute to capillary PVS function, and finally test pericyte and capillary PVS function in aging.

Aim1, I will test the hypothesis that fluid flow in the capillary PVS is directional, following the same direction of blood flow, similar to CSF flow in arterial PVSs. I will utilize in vivo 2-photon imaging of secreted fluorescent protein to label capillary PVSs and measure fluorescent recovery after photobleaching.

Aim 2 will test whether pericytes play a role in clearing waste or maintaining the structure of the capillary PVS. I will use approaches developed in Aim 1 combined with inducible genetic manipulations of pericytes to ablate them or impair their phagocytic and cell matrix maintaining functions, then measure capillary PVSs and glymphatic flow.

Aim3, I will test the hypothesis that capillary PVSs and pericyte dysfunction contribute to glymphatic impairment. I will use the same methods to label capillary PVSs to determine if functional fluid flow decreases, the structure of capillary PVSs changes, or pericyte functions decrease in a cohort of aged mice. I will then attempt to rescue pericyte function in aged mice using PDGF-beta supplementation to improve glymphatic function.

Ultimately this project will answer longstanding questions concerning function of pericapillary PVSs and pericytes, and determine their effect on the glymphatic system in normal aging.

 Feb 08, 2023 @ 2:00 p.m.

 Medical Center | Ryan Case Method (1-9576)

NSC 503 Seminars

Catalina Guzman; Leslie Gonzales - PhD Candidate, Neuroscience Graduate Program

Faculty Evaluators: Anne Luebke & Chris Proschel

 Feb 06, 2023 @ 4:00 p.m.

 Medical Center | K-307

Immunomodulatory approaches to Alzheimer’s Disease

Berke Karaahmet - PhD Candidate in Neuroscience, Advisor: Kerry O’Banion, MD, PhD

Alzheimer’s Disease (AD) is a chronic neurodegenerative disorder that clinically manifests as the most common form of dementia. Due to their surveillance functions and immunocompetence as resident macrophages of the Central Nervous System (CNS), microglia are well-equipped to respond to perturbation of tissue homeostasis. Therefore, they are regarded as promising translational targets in modulating the impact of amyloid and Tau pathologies observed in AD. Here, we sought to elucidate the effect of two peripherally administrated pharmacologic approaches that are hypothesized to modulate microglial activation phenotypes in AD-like models.

In our first approach, we investigated the use of the multiple sclerosis (MS) drug, Glatiramer Acetate (GA), in murine models of aggressive amyloid pathology (5xFAD) or amyloid and Tau pathology combined (3xTg). In response to GA treatment, we observed improvements in cognitive function and molecular pathology in female 3xTg mice. These were associated with minimal transcriptomic changes in microglia, in which Dcstamp was the most upregulated gene. Follow-up analyses of Aβ plaque burden in 5xFAD; DCSTAMP knockout mice showed that the females of this genotype had increased plaque numbers, but this effect did not reach significance. In female 5xFAD mice, we found that GA treatment did not impact plaque burden if started early in life, showed a trend towards decreased plaque burden if started during early disease progression and, unexpectedly, increased plaque burden if started during late disease stages. No changes in plaque burden were observed in 5xFAD males.

In our second approach, we sought to investigate whether microglia that were depleted with a CSF1R inhibitor containing diet and allowed to repopulate could attenuate levels of pathological markers in aged 3xTg mice. We observed no changes in amyloid pathology but found differential effects in several markers of phosphorylated Tau. Single-cell transcriptomic analysis of microglia revealed a cluster that was strongly characterized by Cxcl13 expression. In situ analysis of Cxcl13 showed that it was localized to regions of AD-like pathology in 3xTg mice. This suggests that Cxcl13 upregulation in repopulated microglia responding to AD-like pathology might be one of the driving factors behind the changes observed in phosphorylated Tau levels. Further studies are warranted to establish mechanistic links between these observations.

Altogether, our data indicate that immunomodulatory therapeutics may be beneficial in restricting certain aspects of AD pathology. However, caution must be exercised when designing these therapies since outcomes may depend on the pathological stage of AD.

 Feb 01, 2023 @ 12:00 p.m.

 Medical Center | 1-7619 (Lower Adolph Auditorium)

Host: Dr. Kerry O’Banion, Neuroscience, University of Rochester School of Medicine & Dentistry

NSC 503 Seminars

Mark Osabutey; Sean Lydon - PhD Candidate, Neuroscience Graduate Program

Titles:  The role of Gpnmb in glaucoma - Lydon
Investigrating the effect of NLRP3 inflammasome inhibitor MCC950 on radiation-induced neuroinflammation - Osbutey

Faculty Evaluators: Paul Kammermeir & Amy Kiernan

 Jan 30, 2023 @ 4:00 p.m.

 Medical Center | K-307

NSC 503 Seminars

Caitlin Sharp; Sarah Yablonski - PhD Candidate, Neuroscience Graduate Program

Titles:  "Mapping of threat and reward in trauma exposed individuals" - Sharp
"The role of MKK4 and MKK7 in retinal ganglion cells following acute axonal injury" - Yablonski

Faculty Evaluators: Ken Henry & Manuel Gomez-Ramirez

 Jan 23, 2023 @ 4:00 p.m.

 Medical Center | K-307

The Elizabeth Doty Lecture: Gamma Oscillations, Long-range Inhibition And Prefrontal-Dependent Cognition

Vikaas Sohal, MD, PhD - Associate Professor, Psychiatry, Weill Institute for Neurosciences
University of California at San Francisco

Gamma-frequency (~30-100 Hz) oscillations are observed in many brain regions under many conditions and are known to be deficient in conditions such as schizophrenia. Nevertheless, there has been a robust debate in systems neuroscience about whether gamma oscillations are epiphenomenal or play critical roles in supporting brain function. Correspondingly it’s unclear whether gamma deficits are biomarkers for circuit abnormalities vs key mechanisms that should be targeted to treat disorders such as schizophrenia. Here I will discuss recent published and unpublished work from our lab showing that in mice, gamma synchrony plays a critical role in prefrontal-dependent cognition, can be targeted to remediate cognitive deficits, and emerges from specific interneuron circuits.

 Jan 12, 2023 @ 4:00 p.m.

 Medical Center | 3-7619 Upper Auditorium

Host: The University of Rochester School of Medicine and Dentistry Department of Neuroscience and the Del Monte Institute for Neuroscience