Keck School Faculty

Thomas H. Mc Neill, PhD
Thomas H. Mc Neill, PhD
Professor of Cell & Neurobiology
Integrative Anatomical Sciences
BMT 305D 1333 San Pablo Street Health Sciences Campus Los Angeles
Research Overview
The overall goal of Dr. McNeill's research program is to define the cellular mechanisms that regulate the ability of the brain to repair itself in response to injury (i.e. neuroplasticity) and the effect of aging on these processes. In particular, we wish to further our understanding of the cellular events underlying the synergism between neural plasticity and treatment strategies that promote the recovery of function after brain damage. Understanding the cellular mechanisms that promote neuroplasticity after brain injury is critical for determining the limits of functional recovery that can be expected in brain injured patients, and the first step in developing novel treatment strategies to facilitate the recovery of function after brain injury. Likewise, the ability to manipulate neurotrophrin and neurotransmitters pathways that are activated in response to injury offers a unique opportunity for the development of novel therapies that target a specific cellular mechanisms by translating the fundemental principles of neuroplasticty into effective clinical interventions. The knowledge gained from our studies has relevance for the treatment of neuropsychiatric disorders commonly associated with brain injury as well as in the treatment of neurological deficits associated with Parkinson's disease, Alzheimer's disease, schizophrenia and stroke

Laminin-1 induces endocytosis of 67KDa laminin receptor and protects Neuroscreen-1 cells against death induced by serum withdrawal Biochem Biophys Res Commun. 2018 01 01; 495(1):230-237. . View in PubMed

Polyphenols from green tea prevent antineuritogenic action of Nogo-A via 67-kDa laminin receptor and hydrogen peroxide J Neurochem. 2015 Jan; 132(1):70-84. . View in PubMed

Green tea catechins potentiate the neuritogenic action of brain-derived neurotrophic factor: role of 67-kDa laminin receptor and hydrogen peroxide Biochem Biophys Res Commun. 2014 Feb 28; 445(1):218-24. . View in PubMed

Unilateral skill acquisition induces bilateral NMDA receptor subunit composition shifts in the rat sensorimotor striatum Brain Res. 2013 Jun 23; 1517:77-86. . View in PubMed

Methods for studying oxidative regulation of protein kinase C Methods Enzymol. 2013; 528:79-98. . View in PubMed

Green tea polyphenols precondition against cell death induced by oxygen-glucose deprivation via stimulation of laminin receptor, generation of reactive oxygen species, and activation of protein kinase Ce J Biol Chem. 2012 Oct 05; 287(41):34694-708. . View in PubMed

Green tea polyphenols potentiate the action of nerve growth factor to induce neuritogenesis: possible role of reactive oxygen species J Neurosci Res. 2010 Dec; 88(16):3644-55. . View in PubMed

A direct redox regulation of protein kinase C isoenzymes mediates oxidant-induced neuritogenesis in PC12 cells J Biol Chem. 2008 May 23; 283(21):14430-44. . View in PubMed

Synapse replacement in the striatum of the adult rat following unilateral cortex ablation J Comp Neurol. 2003 Dec 01; 467(1):32-43. . View in PubMed

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