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Efficacy and Safety of Sulforaphane Added to Antipsychotics for the Treatment of Negative Symptoms of Schizophrenia: A Randomized Controlled Trial.
J Clin Psychiatry
January 2025
Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, and Department of Psychiatry, New York University School of Medicine, New York, New York.
There are few established treatments for negative symptoms in schizophrenia, which persist in many patients after positive symptoms are reduced. Oxidative stress, inflammation, and epigenetic modifications involving histone deacetylase (HDAC) have been implicated in the pathophysiology of schizophrenia. Sulforaphane has antioxidant properties and is an HDAC inhibitor.
View Article and Find Full Text PDFp53 mediated regulation of LINE1 retrotransposon derived R-loops.
J Biol Chem
January 2025
Department of Biological Sciences, Indian Institute of Science Education and Research Berhampur, India. Electronic address:
Long Interspersed Nuclear Element 1 (LINE1/L1) retrotransposons, which comprise 17% of the human genome, typically remain inactive in healthy somatic cells but are reactivated in several cancers. We previously demonstrated that p53 silences L1 transposons in human somatic cells, potentially acting as a tumor-suppressive mechanism. However, the precise molecular mechanisms underlying p53-mediated repression of L1 and its life cycle intermediates remain unclear.
View Article and Find Full Text PDFDevelopment of the First-in-Class FEM1B-Recruiting Histone Deacetylase Degraders.
J Med Chem
January 2025
Department of Pharmaceutical and Cell Biological Chemistry, Pharmaceutical Institute, University of Bonn institution, An der Immenburg 4, Bonn 53121, Germany.
Targeted protein degradation (TPD) represents a promising alternative to conventional occupancy-driven protein inhibition. Despite the existence of more than 600 E3 ligases in the human proteome, so far only a few have been utilized for TPD of histone deacetylases (HDACs), which represent important epigenetic anticancer drug targets. In this study, we disclose the first-in-class Fem-1 homologue B (FEM1B)-recruiting HDAC degraders.
View Article and Find Full Text PDFPhase 2A Proof-of-Concept Double-Blind, Randomized, Placebo-Controlled Trial of Nicotinamide in Early Alzheimer Disease.
Neurology
January 2025
From the Institute for Memory Impairments and Neurological Disorders (J.D.G., S.T., G.T., B.V., K.G., D.L.G.), University of California, Irvine; Department of Psychiatry and Human Behavior (J.D.G.), University of California, Irvine; Department of Neurobiology and Behavior (J.D.G., K.G.), University of California, Irvine; Division of Geriatric Medicine (S.T.), Department of Medicine, University of California, Irvine; Department of Neurology (G.T.), University of California, Irvine; Department of Neurology (A.L.P.), Oregon Health and Science University; Department of Statistics (D.L.G.), University of California, Irvine; Department of Neurology and Neurological Sciences (E.T.), Stanford University; Department of Neurology (S.K.), Cedars Sinai Medical Center; Department of Neurology (M.B.), University of California, Los Angeles; Alzheimer's Disease Cooperative Study (R.A.R., G.C.L., A.B., C.R., R.M., R.J., J.P., J.Z., S.J., K.M., H.H.F.), University of California, San Diego; and Department of Neurosciences (G.C.L., J.P., H.H.F.), University of California, San Diego.
Background And Objectives: Nicotinamide is a coenzyme involved in cellular oxidation-reduction reactions that can inhibit Class III histone deacetylases (HDACs) or sirtuins. HDAC inhibition can affect numerous therapeutic pathways, including tau phosphorylation. We tested the hypothesis that nicotinamide treatment could reduce tau phosphorylation in early Alzheimer disease (AD).
View Article and Find Full Text PDFAnemia of Inflammation is a prevalent co-morbidity in patients with chronic inflammatory disorders. Inflammation causes hypoferremia and iron-restricted erythropoiesis by limiting Ferroportin (FPN)-mediated iron export from macrophages that recycle senescent erythrocytes. Macrophage cell surface expression of FPN is reduced by hepcidin-induced degradation and/or by repression of FPN (Slc40a1) transcription via cytokine and Toll-like receptor (TLR) stimulation.
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