Seminar Series - Fall 2022

September 19 , 2022 : CBNP Seminar (Student Hosted Seminar)– Dr. Marco Venniro, University of Maryland
Title: "Social reward to protect against substance use disorders"
Host: Hunter Lanovoi

Abstract: The goal of our research, and of the addiction field in general, has not merely been to identify neuropharmacological and circuit mechanisms of drug addiction and relapse. The goal was to achieve prospective predictive validity—the ability to identify new treatments. As I will describe in the lecture, the classical relapse model in its traditional form has not appreciably changed the options available to patients in need of relapse prevention. This shortcoming is not unique to relapse, but it is an increasing source of disappointment, and it calls for a regrouping.

In our laboratory, we have regrouped by developing a set of approaches that begin with reverse translation. As a first step, we have mimicked behavioral treatments that are largely successful in humans: contingency management, and community-reinforcement approach. None of these treatments is universally effective in the clinic, and, this, too, can be modelled in our rats. These reverse-translated “treatments” are an ecologically relevant platform from which we can move on to translation itself, using different methods to discover new relapse-related circuits and to identify new medications for relapse prevention in “treated” or post-“treated” rats. In the lecture, I will introduce these animal models, describe our initial pharmacological and circuit results, and discuss implications for treatment.

Bio: Marco received a Ph.D. in pharmacology from the University of Palermo in 2012. He was then accepted into the NIH Graduate Partnership Program. Following a 2-year fellowship at the National Institute on Drug Abuse Marco received his Ph.D. in translational biomedicine from the University of Verona in 2016. He completed his postdoctoral fellowship in the laboratory of Dr. Yavin Shaham in 2020. He joined the University of Maryland School of Medicine as an assistant professor in the Department of Anatomy and Neurobiology in 2021.

Marco is interested in behavior and translational research with a focus on the social component of neuropsychiatric disorders. He is particularly interested in understanding how alternative nondrug rewards can be used to control and treat drug addiction with a focus on social reward.

Recommend Readings:

https://www.nature.com/articles/s41593-018-0246-6

https://pubmed.ncbi.nlm.nih.gov/32205443/

 

September 26, 2022: PPN Department Seminar– Dr. Laibaik Park, Weill Cornell Medical College
Title: "Towards a mechanistic understanding of the neurovascular dysfunction of Alzheimer’s disease"
Host: Hyung Jin Ahn, Ph.D.

Abstract: Neurovascular dysfunction plays a pathogenic role in neurodegenerative diseases, including Alzheimer’s disease (AD) and frontotemporal dementia (FTD). Amyloid-β (Aβ) and tau, peptides centrally involved in the pathogenesis of AD and/or FTD, have profound neurovascular effects. I will discuss work from our lab to investigate mechanistic pathways by which Aβ and tau impair neurovascular regulation. Our work is revealing that neurovascular dysfunction is an early pathogenic contributor to the disease progress and is generating important considerations for counteracting the neuronal dysfunction underlying the cognitive impairment in AD and FTD patients.

References:

1. Park L, Hochrainer K, Hattori Y, Ahn SJ, Anfray A, Wang G, Uekawa K, Seo J, Palfini V, Blanco I, Acosta D, Eliezer D, Zhou P, Anrather J, Iadecola C (2020). Tau induces PSD95-neuronal NOS uncoupling and neurovascular dysfunction independent of neurodegeneration. Nat Neurosci. 23(9):1079-1089.

2. Park L, Uekawa K, Garcia-Bonilla L, Koizumi K, Murphy M, Pistik R, Younkin L, Younkin S, Zhou P, Carlson G, Anrather J, Iadecola C (2017). Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides. Circ Res. 121(3):258-269.

3. Koizumi K, Wang G, Park L (2016). Endothelial Dysfunction and Amyloid-β-Induced Neurovascular Alterations. Cell Mol Neurobiol. 36(2):155-65.

 

October 3, 2022: PPN Department Seminar - Dr. Michael Krashes, NIDDK
Title: TBA
Host: Ioana Carcea, Ph.D.

 

October 10, 2022 : CBNP Seminar Anesthesiology – Dr. Ru-Rong Ji, Duke University
Title: TBA
Host: YX Pan, Ph.D.

 

October 17, 2022 : PPN Department Seminar – Dr. Hervé Boutin, University of Manchester
Title: TBA
Host: Hyung Jin Ahn, Ph.D.

 

October 24, 2022 : CBNP Seminar CBMM – Dr. Tomas Falzone, CONICET, Argentina
Title: "Novel players in axonal transport regulation, DYRK1A modifying the bidirectional movement of APP in human derived neurons"
Host: Diego Fraidenraich, Ph.D.

DYRK1A triplication in Down’s Syndrome (DS) and its overexpression in Alzheimer’s Disease (AD) suggest a role for increased DYR1A activity in the abnormal metabolism of APP. Transport defects are early phenotypes in the progression of AD, which lead to APP processing impairments. However, whether DYRK1A regulates the intracellular transport and delivery of APP in human neurons remains unknown. From a proteomic dataset of human cerebral organoids treated with harmine, a DYRK1A inhibitor, we found expression changes in protein clusters associated with the control of microtubule-based transport and in close interaction with the APP vesicle. Live-imaging of APP axonal transport in human-derived neurons treated with harmine or overexpressing a dominant negative DYRK1A revealed a reduction in APP vesicle density and enhanced the stochastic behavior of retrograde vesicle transport. Moreover, harmine increased the fraction of slow segmental velocities and changed speed transitions supporting a DYRK1A-mediated effect in the exchange of active motor configuration. Contrarily, the overexpression of DYRK1A in human polarized neurons increased the axonal density of APP vesicles and enhanced the processivity of retrograde APP. In addition, increased DYRK1A activity induced faster retrograde segmental velocities together with significant changes in slow to fast anterograde and retrograde speeds transitions. Our results highlight DYRK1A as a modulator of the axonal transport machinery driving APP intracellular distribution in neurons, and stress DYRK1A inhibition as a putative therapeutic intervention to restore APP axonal transport in DS and AD.

 

 

October 31, 2022: PPN Department Seminar – Dr. Vadim Ten, RWJMS Rutgers University
Title: "Cyclophilin D dependent mitochondrial proton leak contributes to oligodendrocytes maturation failure and diffuse white matter hypomyelination in neonatal mice"
Host: Steven Levison, Ph.D.

 

November 7, 2022 : NoSeminar

November 14, 2022: NoSeminar

November 21, 2022: CBNP Seminar CBMM - Dr. Nazish Sayed, Stanford University
Title: TBA
Host: Maha Abdellatif

November 28, 2022: NoSeminar

December 5, 2022: CBNP Seminar Anesthesiology Dr. Rajesh Khanna, NYU
Title: TBA
Host: Dr. Hu

How are synaptic networks formed during development and remodelled during learning and disease? This is the main question that drives our research. In particular, we investigate the roles ofglial cells called astrocytes in the development, remodelling and function of synaptic circuits.In my talk, I will share findings from my lab on two distinct molecular mechanisms through which astrocytes control synapse formation and discuss how synaptogenic astrocyte signals are critical for proper development and function of the nervous system.

 

December 12, 2022: PPN Department Seminar – Dr. Tara DeSilva, the Cleveland Clinic
Title: TBA
Host: Terri Wood, Ph.D.

 

December 19 2022: No Seminar