Hala Nicolas, PhD Email Hala Nicolas
- ASSISTANT PROFESSOR | Psychiatry
- ASSISTANT PROFESSOR (PENDING) | Neuroscience
Dr. Harony-Nicolas is an Assistant Professor at the Department of Psychiatry and a Seaver Fellow at the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai. She is a molecular and behavioral neuroscientist with extensive skills and expertise in studying transgenic rodent models for neurodevelopmental disorders, mainly Phelan McDerimd Syndrome (PMS) and autism spectrum disorder (ASD). She received her PhD in Molecular Biology at the Technion Institute in Israel and completed her first postdoctoral training in Molecular Neurobiology at University of Haifa, Israel. In the fall of 2011, she joined Dr. Joseph Buxbaum’s laboratory and the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai, where she completed her second post-doctoral training and was promoted to the level of Instructor in 2014. Her postdoctoral training lead to the validation and characterization for a new transgenic rat model for ASD; the Shank3-deficient rat, and for the demonstration that an acute administration of the oxytocin peptide ameliorates the synaptic plasticity, social memory, and attentional deficits, we observed in this model (Harony-Nicolas et al., eLife, 2017).
Dr. Harony-Nicolas’s research is focused on understanding the mechanisms by which ASD-associated mutations lead to the manifestation of behavioral deficits, with an emphasis on the effect of these mutations on the brain oxytocin system, known as a major modulator of mammalian social behavior, and on brain circuits of social behavior. Her lab applies integrated molecular and behavioral neuroscience approaches and uses transgenic rat models for ASD and neurodevelopmental disorders to identify molecular targets for treatment and to uncover altered brain circuits that can be manipulated with circuit-specific non-invasive interventions.
BSc, Technion - Israel Institute of Technology
MA, Technion - Israel Institute of Technology
PhD, Technion - Israel Institute of Technology
Dr. Harony-Nicolas’s research aims to understand the mechanisms underlying the pathogenesis of autism spectrum disorder (ASD) by using transgenic ASD rat models and applying behavioral and molecular neuroscience approaches, genome wide transcriptional analysis, and cutting-edge chemo-genetic tools. The long-term goal of her laboratory is to identify molecular targets for treatment and to uncover altered brain circuits that can be manipulated with circuit-specific non-invasive interventions.
Dr. Harony-Nicolas’s has recently characterized and validated a novel genetically modified rat model for ASD, the Shank3-deficient rats, and has demonstrated that the pro-social peptide oxytocin ameliorates behavioral and physiological deficits in this model (Harony-Nicolas et al., eLife, 2017). Her current studies are focused on unraveling the effect of ASD associated mutation on the oxytocin brain system and on brain circuits of social behavior leading to social behavior deficits.
Harony-Nicolas H, Kay M, Hoffmann JD, Klein ME, Bozdagi-Gunal O, Riad M, Daskalakis NP, Sonar S, Castillo PE, Hof PR, Shapiro ML, Baxter MG, Wagner S, Buxbaum JD. Oxytocin improves behavioral and electrophysiological deficits in a novel Shank3-deficient rat. eLife 2017 Jan; 6.
Varghese M, Keshav N, Jacot-Descombes S, Warda T, Wicinski B, Dickstein DL, Harony-Nicolas H, De Rubeis S, Drapeau E, Buxbaum JD, Hof PR. Autism spectrum disorder: neuropathology and animal models. Acta neuropathologica 2017 Jun;.
Hsiao K, Harony-Nicolas H, Buxbaum JD, Bozdagi-Gunal O, Benson DL. Cyfip1 Regulates Presynaptic Activity during Development. The Journal of neuroscience : the official journal of the Society for Neuroscience 2016 Feb; 36(5).
Harony-Nicolas H, De Rubeis S, Kolevzon A, Buxbaum JD. Phelan McDermid Syndrome: From Genetic Discoveries to Animal Models and Treatment. Journal of child neurology 2015 Dec; 30(14).
Uppal N, Puri R, Yuk F, Janssen WG, Bozdagi-Gunal O, Harony-Nicolas H, Dickstein DL, Buxbaum JD, Hof PR. Ultrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice. Molecular autism 2015; 6.
Harony-Nicolas H, Mamrut S, Brodsky L, Shahar-Gold H, Barki-Harrington L, Wagner S. Brain region-specific methylation in the promoter of the murine oxytocin receptor gene is involved in its expression regulation. Psychoneuroendocrinology 2014 Jan; 39.
Poultney CS, Goldberg AP, Drapeau E, Kou Y, Harony-Nicolas H, Kajiwara Y, De Rubeis S, Durand S, Stevens C, Rehnström K, Palotie A, Daly MJ, Ma'ayan A, Fromer M, Buxbaum JD. Identification of small exonic CNV from whole-exome sequence data and application to autism spectrum disorder. American journal of human genetics 2013 Oct; 93(4).
Mamrut S, Harony H, Sood R, Shahar-Gold H, Gainer H, Shi YJ, Barki-Harrington L, Wagner S. DNA methylation of specific CpG sites in the promoter region regulates the transcription of the mouse oxytocin receptor. PloS one 2013; 8(2).
Harony H, Wagner S. The contribution of oxytocin and vasopressin to mammalian social behavior: potential role in autism spectrum disorder. Neuro-Signals 2010; 18(2).
Harony H, Ankri S. What do unicellular organisms teach us about DNA methylation?. Trends in parasitology 2008 May; 24(5).
Lavi T, Isakov E, Harony H, Fisher O, Siman-Tov R, Ankri S. Sensing DNA methylation in the protozoan parasite Entamoeba histolytica. Molecular microbiology 2006 Dec; 62(5).
Harony H, Bernes S, Siman-Tov R, Ankri S. DNA methylation and targeting of LINE retrotransposons in Entamoeba histolytica and Entamoeba invadens. Molecular and biochemical parasitology 2006 May; 147(1).
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Dr.Nicolas did not report having any of the following types of financial relationships with industry during 2018 and/or 2019: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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