Feil Family Brain & Mind Research Institute

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Park, Laibaik - Iadecola Laboratory - Neurovascular Pathologies and Neurodegeneration

Laibaik Park, Ph.D.
Assistant Professor of Neuroscience

Overview

The brain is one of the most essential and delicate organs in the body. Flawless functioning of the brain depends on a functionally integrated neurovascular network, termed a neurovascular unit. The neurovascular unit, formed by neurons, glia (astrocytes, microglia, and perivascular macrophages), and vascular cells (endothelial cells and smooth cells), plays a critical role in supplying nutrients to and draining waste products out of the brain. The focus of my laboratory's work is to understand how neurovascular units are anatomically/functionally integrated, what neurovascular factors are involved in the neurovascular integration, and how neurovascular units control blood flow to the brain. To implement findings in basic research, we also investigate how alterations in the neurovascular units underlie cerebrovascular and neurodegenerative diseases, including cerebral ischemia and Alzheimer’s disease. Therefore, my lab’s goals are to understand (1) how neurovascular factors, especially tissue plasminogen activator, drive neurovascular regulation, (2) how amyloid and tau, two major culprits in Alzheimer’s dementia, alters the neurovascular regulation, and (3) how alterations in the neurovascular coupling contribute to brain dysfunctions, including the dementia in Alzheimer’s disease.

Achievements & Publications

  • Park L, Zhou J, Zhou P, Pitstick R, El Jamal S, Younkin L, Pierce J, Arreguin A, Anrather J, Younkin SG, Carlson GA, McEwen BS, & Iadecola C. The innate immunity receptor CD36 promotes cerebral amyloid angiopathy. Proc Natl Acad Sci USA, 110: 3089-3094, 2013.
  • Park L, Zhou P, Koizumi K, El Jamal S, Previti ML, Van Nostrand WE, Carlson GA, & Iadecola C. Brain and circulating levels of Aβ1-40 differently contribute to vasomotor dysfunction in the mouse brain. Stroke, 44:198-204, 2013. 
  • Wang G, Coleman C, Glass M, Zhou P, Yu Q, Park L, Anrather J, Pickel V, and Iadecola C. Angiotensin II type 2 receptor-coupled nitric oxide production modulates free radical availability and voltage-gated Ca2+ currents in NTS neurons. Am J Physiol (Regul Integr Com Physiol), 302:R1076-R1083, 2012.
  • Park L, Wang G, Zhou P, Zhou J, Pitstick R, Previti ML, Younkin L, Younkin SG, Van Nostrand WE, Cho S, Anrather J, Carlson GA, & Iadecola C. Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-β. Proc Natl Acad Sci USA, 108:5063-5068, 2011. 
  • Capone C, Faraco G, Park L, Cao X, Davisson R, and Iadecola C. The cerebrovascular dysfunction induced by slow pressor doses of angiotensin-II precedes the development of hypertension. Am J Physiol, 300:H397-407, 2011.
  • Coleman C, Wang G, Park L, Anrather J, Delagrammatikas G, Chan J, Zhou J, Iadecola C, and Pickel V. Chronic intermittent hypoxia induces NMDA receptor-dependent plasticity and suppresses nitric oxide signaling in the mouse hypothalamic paraventricular nucleus. J Neurosci, 30:12103-12112, 2010.
  • Park L, Zhou P, Pitstick R, Capone C, Anrather J, Norris EH, Younkin L, Younkin  S, Carlson G, McEwen BS, & Iadecola C. Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein. Proc Natl Acad Sci USA, 105:1347-1352, 2008. 
  • Park L, Gallo EF, Anrather J, Wang G, Norris EH, Paul J, Strickland S, & Iadecola C. Key role of tissue plasminogen activator in neurovascular coupling. Proc Natl Acad Sci USA, 105:1073-1078, 2008.

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