Search

Your search keyword '"Cheyette BNR"' showing total 6 results
Start Over Author "Cheyette BNR" Publication Year Range Last 10 years
6 results on '"Cheyette BNR"'

1. DIXDC1 contributes to psychiatric susceptibility by regulating dendritic spine and glutamatergic synapse density via GSK3 and Wnt/β-catenin signaling

Author

Martin, P-M, Stanley, RE, Ross, AP, Freitas, AE, Moyer, CE, Brumback, AC, Iafrati, J, Stapornwongkul, KS, Dominguez, S, Kivimäe, S, Mulligan, KA, Pirooznia, M, McCombie, WR, Potash, JB, Zandi, PP, Purcell, SM, Sanders, SJ, Zuo, Y, Sohal, VS, and Cheyette, BNR

Subjects
Biological Psychology, Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Psychology, Mental Illness, Depression, Serious Mental Illness, Neurosciences, Behavioral and Social Science, Brain Disorders, Mental Health, 2.1 Biological and endogenous factors, Mental health, Animals, Anxiety, Anxiety Disorders, Dendritic Spines, Depressive Disorder, Glutamate Plasma Membrane Transport Proteins, Glycogen Synthase Kinase 3, Intracellular Signaling Peptides and Proteins, Mental Disorders, Mice, Mice, Knockout, Polymorphism, Single Nucleotide, Pyramidal Cells, Social Behavior, Synapses, Wnt Signaling Pathway, beta Catenin, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

Mice lacking DIX domain containing-1 (DIXDC1), an intracellular Wnt/β-catenin signal pathway protein, have abnormal measures of anxiety, depression and social behavior. Pyramidal neurons in these animals' brains have reduced dendritic spines and glutamatergic synapses. Treatment with lithium or a glycogen synthase kinase-3 (GSK3) inhibitor corrects behavioral and neurodevelopmental phenotypes in these animals. Analysis of DIXDC1 in over 9000 cases of autism, bipolar disorder and schizophrenia reveals higher rates of rare inherited sequence-disrupting single-nucleotide variants (SNVs) in these individuals compared with psychiatrically unaffected controls. Many of these SNVs alter Wnt/β-catenin signaling activity of the neurally predominant DIXDC1 isoform; a subset that hyperactivate this pathway cause dominant neurodevelopmental effects. We propose that rare missense SNVs in DIXDC1 contribute to psychiatric pathogenesis by reducing spine and glutamatergic synapse density downstream of GSK3 in the Wnt/β-catenin pathway.

Published
2018

2. This title is unavailable for guests, please login to see more information.

Author

Martin, P-M, Martin, P-M, Stanley, RE, Ross, AP, Freitas, AE, Moyer, CE, Brumback, AC, Iafrati, J, Stapornwongkul, KS, Dominguez, S, Kivimäe, S, Mulligan, KA, Pirooznia, M, McCombie, WR, Potash, JB, Zandi, PP, Purcell, SM, Sanders, SJ, Zuo, Y, Sohal, VS, Cheyette, BNR, Martin, P-M, Martin, P-M, Stanley, RE, Ross, AP, Freitas, AE, Moyer, CE, Brumback, AC, Iafrati, J, Stapornwongkul, KS, Dominguez, S, Kivimäe, S, Mulligan, KA, Pirooznia, M, McCombie, WR, Potash, JB, Zandi, PP, Purcell, SM, Sanders, SJ, Zuo, Y, Sohal, VS, and Cheyette, BNR

Published
2018

3. Neurodevelopmental Perspectives on Wnt Signaling in Psychiatry

Author

Mulligan, KA and Cheyette, BNR

Abstract

Mounting evidence indicates that Wnt signaling is relevant to pathophysiology of diverse mental illnesses including schizophrenia, bipolar disorder, and autism spectrum disorder. In the 35 years since Wnt ligands were first described, animal studies have richly explored how downstream Wnt signaling pathways affect an array of neurodevelopmental processes and how their disruption can lead to both neurological and behavioral phenotypes. Recently, human induced pluripotent stem cell (hiPSC) models have begun to contribute to this literature while pushing it in increasingly translational directions. Simultaneously, large-scale human genomic studies are providing evidence that sequence variation in Wnt signal pathway genes contributes to pathogenesis in several psychiatric disorders. This article reviews neurodevelopmental and postneurodevelopmental functions of Wnt signaling, highlighting mechanisms, whereby its disruption might contribute to psychiatric illness, and then reviews the most reliable recent genetic evidence supporting that mutations in Wnt pathway genes contribute to psychiatric illness. We are proponents of the notion that studies in animal and hiPSC models informed by the human genetic data combined with the deep knowledge base and tool kits generated over the last several decades of basic neurodevelopmental research will yield near-term tangible advances in neuropsychiatry.

Published
2017
Full Text
View/download PDF

4. Acute exacerbation of irritable bowel syndrome prevented by prn oral triptan

Author

Cheyette, BNR and Cheyette, SNR

Subjects
Irritable Bowel Syndrome, Diagnosis, Differential, Male, Gastrointestinal Agents, digestive, oral, and skin physiology, Acute Disease, Humans, Administration, Oral, Middle Aged, Tryptamines
Abstract

We report a case of irritable bowel syndrome (IBS), diarrhea subtype, characterized by daily 'morning rush' and episodic acute exacerbations brought on by common IBS trigger foods including insoluble fiber, red wine and large/rich meals. The patient also had a history of migraine headaches, and a family history suggesting a common diathesis for both disorders. Given hypothesized contributions to IBS from dysregulation of the enteric serotonergic system, a trial of low-dose triptan medication was implemented in the context of the patient's known IBS triggers, with highly satisfactory results.

Published
2016
Full Text
View/download PDF

5. Enhancing WNT Signaling Restores Cortical Neuronal Spine Maturation and Synaptogenesis in Tbr1 Mutants.

Author

Fazel Darbandi S, Robinson Schwartz SE, Pai EL, Everitt A, Turner ML, Cheyette BNR, Willsey AJ, State MW, Sohal VS, and Rubenstein JLR

Subjects
Animals, Autism Spectrum Disorder genetics, DNA-Binding Proteins metabolism, Dendritic Spines physiology, Female, HEK293 Cells, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Neurogenesis physiology, Neurons metabolism, Neurons physiology, Synapses metabolism, T-Box Domain Proteins genetics, T-Box Domain Proteins physiology, Thalamus metabolism, Wnt Signaling Pathway genetics, Dendritic Spines metabolism, T-Box Domain Proteins metabolism, Wnt Signaling Pathway physiology
Abstract

Tbr1 is a high-confidence autism spectrum disorder (ASD) gene encoding a transcription factor with distinct pre- and postnatal functions. Postnatally, Tbr1 conditional knockout (CKO) mutants and constitutive heterozygotes have immature dendritic spines and reduced synaptic density. Tbr1 regulates expression of several genes that underlie synaptic defects, including a kinesin (Kif1a) and a WNT-signaling ligand (Wnt7b). Furthermore, Tbr1 mutant corticothalamic neurons have reduced thalamic axonal arborization. LiCl and a GSK3β inhibitor, two WNT-signaling agonists, robustly rescue the dendritic spines and the synaptic and axonal defects, suggesting that this could have relevance for therapeutic approaches in some forms of ASD., Competing Interests: Declaration of Interests J.L.R.R. is cofounder and stockholder, and currently on the scientific board, of Neurona, a company studying the potential therapeutic use of interneuron transplantation. A.J.W. is a paid consultant for Daiichi Sankyo. M.W.S. is a consultant to BlackThorn and ArRett Pharmaceuticals. All other authors declare no competing interests., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results