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Vilma Gabbay

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  63
Citations -  2453

Vilma Gabbay is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Anhedonia & Major depressive disorder. The author has an hindex of 24, co-authored 55 publications receiving 2027 citations. Previous affiliations of Vilma Gabbay include New York University & Nathan Kline Institute for Psychiatric Research.

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A preliminary study of functional connectivity in comorbid adolescent depression.

TL;DR: Functional connectivity data suggest that MDD in adolescence is associated with abnormal connectivity within neural circuits that mediate emotion processing, and hypothesis-driven, seed-based analyses of resting state fMRI data hold promise for advancing current understanding of abnormal development of neural circuitry in adolescents with MDD.
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Striatum-based circuitry of adolescent depression and anhedonia.

TL;DR: Although MDD diagnosis and severity were related to striatal networks involving midline cortical structures, distinct circuits within the reward system were associated with anhedonia, which supports the incorporation of both categorical and dimensional approaches in neuropsychiatric research.
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Anterior cingulate cortex γ-aminobutyric acid in depressed adolescents: relationship to anhedonia.

TL;DR: Findings suggest that GABA, the major inhibitory neurotransmitter in the brain, may be implicated in adolescent MDD and, more specifically, in those with anhedonia.
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Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: evidences from animal and human studies

TL;DR: The role of the kynurenine pathway in the pathophysiology of depression, as well as a novel therapeutic target to classic and new modulators to treat depression based on findings from preclinical and clinical studies are highlighted.
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Immune system dysregulation in adolescent major depressive disorder.

TL;DR: Findings suggest that immune system dysregulation may be associated with adolescent MDD, with an imbalance of Th1/Th2 shifted toward Th1, as documented in adult MDD.