This report of two cases in which schizophrenia and beta-thalassemia occurred simultaneously in several family members may suggest that a genetic link exists between these two disorders. A known genetic disease (beta-thalassemia) could help confirm the presence, on the short arm of chromosome 11, of a genetic susceptibility factor for schizophrenia.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.psychres.2007.11.001 | DOI Listing |
Front Psychiatry
April 2023
Department of Hematology and Oncology, Ningbo No.2 Hospital, Ningbo, China.
A patient with schizophrenia who was treated with chlorpromazine developed lupus anticoagulant (LA) and antiphospholipid syndrome (APS). On protein electrophoresis, a monoclonal immunoglobulin A peak was seen in this patient, defining a condition of monoclonal gammopathy of undetermined significance. Additionally, β-thalassemia was diagnosed with the CD41-42 genotype.
View Article and Find Full Text PDFBMC Med Genet
October 2020
Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, 10 Lavrentyev Ave, Novosibirsk, 630090, Russia.
Background: Hemoglobin is a tetramer consisting of two α-chains and two β-chains of globin. Hereditary aberrations in the synthesis of one of the globin chains are at the root of thalassemia, one of the most prevalent monogenic diseases worldwide. In humans, in addition to α- and β-globins, embryonic zeta-globin and fetal γ-globin are expressed.
View Article and Find Full Text PDFGlycine transporter-1 (GlyT1) inhibition has been extensively studied both in pharmaceutical companies and academic institutions primarily as a potential new approach to treat schizophrenia, a severe and chronic mental illness. More recently, preclinical results have suggested that this approach could also have therapeutic potential for CNS disorders beyond schizophrenia as well as for non-CNS indications. Over the past 17 years, Roche has been a key player in the GlyT1 field with the discovery and development of bitopertin, the most advanced GlyT1 inhibitor to date and the only one which completed Phase III clinical studies for schizophrenia.
View Article and Find Full Text PDFInt J Dev Neurosci
October 2017
Department of Psychiatry, Bakirkoy Education and Research Hospital for Psychiatry, Turkey.
Hemoglobin (Hb) expression in the central nervous system is recently shown. Cooccurences of mental disorders (mainly bipolar disorder (BD) and tic disorders) with β- or α-thalassemia trait or erythrocytosis were witnessed, which may be due to peripheral or central hypoxia/hyperoxia or haplotypal gene interactions. β-Globin genes reside at 11p15.
View Article and Find Full Text PDFA transition from fetal hemoglobin (HbF) to adult hemoglobin (HbA) normally occurs within a few months after birth. Increased production of HbF after this period of infancy ameliorates clinical symptoms of the major disorders of adult β-hemoglobin: β-thalassemia and sickle cell disease. The transcription factor BCL11A silences HbF and has been an attractive therapeutic target for increasing HbF levels; however, it is not clear to what extent BCL11A inhibits HbF production or mediates other developmental functions in humans.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!