Dr. Joshua Kantrowitz is an Assistant Professor of Psychiatry at NYSPI/Columbia University, and the Director of the Lieber Schizophrenia Research Clinic. He is the author of over 40 peer reviewed articles published in internationally recognized journals. His research work has been recognized with the Young Investigator Travel Award by the International Congress of Schizophrenia Research (ICOSR) and the Schizophrenia International Research Society (SIRS) and the Dr. Joseph E. and Lillian Pisetsky Young Investigator Award for Clinical Research in Serious Mental Illness.
In his career, Dr. Kantrowitz has primarily focused on investigating glutamatergic psychopharmacology and treatment for schizophrenia and depression. He has extensive experience conducting pharmacological biomarker studies in his capacity of Director of the Lieber Research Clinic. He has been the principal/co-investigator on several NIMH-funded trials, including the Fast-Fail Trials in Psychotic Spectrum Disorders project which measures changes in glutamatergic neurophysiology using 1H MRS.
He recently published the first demonstration that D-cycloserine, a partial agonist/antagonist at the N-methyl-D-aspartate-type glutamate receptors (NMDAR) may prevent relapse after treatment with the non-competitive NMDAR antagonist ketamine. In a follow up study, he has shown that D-cycloserine induces acute increases in brain glutamate comparable to ketamine, suggesting that 1H MRS can be used for early stage trials of glutamatergic compounds. In collaboration with Dr. Daniel Javitt, he has demonstrated the efficacy of high dose D-serine, a naturally occurring endogenous modulator of NMDAR in both chronic and early (prodromal) schizophrenia.
A second major focus of his career has been to document the existence and profound functional and neurophysiological consequences of early sensory processing deficits to overall and social function. These publications include demonstrations that reduced ability to discriminate simple tones correlates with impairments in emotion recognition, theory of mind and music recognition. Most recently, he demonstrated intercorrelated impairments in early auditory processing that predicted impairment in emotion recognition. He has also demonstrated that sensory level remediation may be beneficial at reversing these deficits, that NMDAR dysfunction may contribute to underlying neuroplasticity deficits and, finally that repeated D-serine administration may enhance neuroplasticity in schizophrenia.
In addition to his primary work with glutamatergic compounds and sensory processing deficits, he has extensive experience leading clinical research projects in psychiatric populations of other novel mechanism agents, including as a site PI for a TURNS network project. These include an ongoing Phase 1b, study of AVL-3288, an allosteric modulator of the a7- nicotinic cholinergic receptor, proof of concept trial of a GABAB agonist for negative symptoms and impaired sleep in schizophrenia, a several studies of the glycine transport inhibitor bitopertin, a Phase III study of the mGlu2/3R agonist LY2140023, and a Phase II study of the histamine-type 3 receptor antagonist GSK239512.