Akiko Sumitomo

ORCID: 0000-0003-3051-0485
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Tryptophan and brain disorders
  • Autophagy in Disease and Therapy
  • Cannabis and Cannabinoid Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Phosphodiesterase function and regulation
  • Nerve injury and regeneration
  • Renin-Angiotensin System Studies
  • Receptor Mechanisms and Signaling
  • Stress Responses and Cortisol
  • Neurotransmitter Receptor Influence on Behavior
  • RNA modifications and cancer
  • Mesenchymal stem cell research
  • MicroRNA in disease regulation
  • Attention Deficit Hyperactivity Disorder
  • Autism Spectrum Disorder Research
  • Dermatology and Skin Diseases
  • Neuroscience and Neuropharmacology Research
  • Congenital heart defects research
  • Endoplasmic Reticulum Stress and Disease
  • Biochemical Analysis and Sensing Techniques
  • Diet and metabolism studies
  • Cancer Cells and Metastasis
  • Treatment of Major Depression
  • Contact Dermatitis and Allergies
  • Cytokine Signaling Pathways and Interactions

Centre for Addiction and Mental Health
2018-2024

University of Toronto
2018-2024

Mental Health Research Institute
2020-2023

Mental Health Research Canada
2020-2021

Kyoto University
2016-2020

Beckman Research Institute
2018

City of Hope
2018

Kyoto Medical Center
2016

Miyazaki International College
2015

RMIT University
2012

Autophagy plays an essential role in intracellular degradation and maintenance of cellular homeostasis all cells, including neurons. Although a recent study reported copy number variation Ulk2, gene for initiating autophagy, associated with case schizophrenia (SZ), it remains to be studied whether Ulk2 dysfunction could underlie the pathophysiology disease. Here we show that heterozygous (Ulk2+/-) mice have upregulated expression sequestosome-1/p62, autophagy-associated stress response...

10.1093/hmg/ddy219 article EN Human Molecular Genetics 2018-06-06

22q11.2 deletions, a genetic risk for schizophrenia, could be susceptible to Parkinson’s disease through elevated expression of α-synuclein.

10.1126/sciadv.aar6637 article EN cc-by-nc Science Advances 2018-08-03

The Mediator subunit MED1 is essential for mammary gland development and lactation, whose contribution through direct interaction with estrogen receptors (ERs) restricted to involvement in pubertal luminal cell differentiation. Here, we provide evidence that the MED24-containing submodule of functionally communicates specifically development. Mammary glands from MED1/MED24 double heterozygous knockout mice showed profound retardation ductal branching during puberty, while single...

10.1128/mcb.05245-11 article EN Molecular and Cellular Biology 2012-02-14

Abstract Aging is associated with reduced brain volume, altered neural activity, and neuronal atrophy in cortical-like structures, comprising the frontal cortex hippocampus, together contributing to cognitive impairments. Therapeutic efforts aimed at reversing these deficits have focused on excitatory or neurotrophic mechanisms, although recent findings show that dendritic inhibition mediated by α5-subunit containing GABA-A receptors (α5-GABAA-Rs) occurs during aging contributes impairment....

10.1093/cercor/bhaa310 article EN Cerebral Cortex 2020-09-22

MED1/TRAP220, a subunit of the transcriptional Mediator/TRAP complex, is crucial for various biological events through its interaction with distinct activators, such as nuclear receptors and GATA family activators. In hematopoiesis, MED1 plays pivotal role in optimal receptor-mediated myelomonopoiesis GATA-1-induced erythropoiesis. this study, we present evidence that stromal cells involved supporting hematopoietic stem and/or progenitor (HSPCs) osteopontin (OPN) expression. We found...

10.1128/mcb.01348-09 article EN Molecular and Cellular Biology 2010-08-17

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental that, while prevalent, has stagnant track record for advances in treatment. The limited availability of animal models with appropriate face and predictive validities hampered progress developing novel neurobiological hypotheses testing new therapeutic options this condition. Here, we report that mice deficient Fez1, gene specifically expressed the nervous system documented functions neurodevelopment, show hyperactivity...

10.1159/000488081 article EN Complex Psychiatry 2017-01-01

ABSTRACT Major Depressive disorder (MDD) is a chronic and recurrent brain characterized by episode remission phases, poor therapeutic responses. The molecular correlates of MDD have been investigated in case-control settings, but the biological changes associated with trait (regardless episode/remission) or state (illness phases) remains largely unknown, hence preventing opportunities. To address this gap, we generated transcriptome profiles subgenual anterior cingulate cortex subjects who...

10.1101/2020.04.24.058610 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-04-27

Although still a matter of controversy, disrupted in schizophrenia protein 1 (DISC1) was suggested as potential inhibitor phosphodiesterase 4 (PDE4). We used Disc1 locus impairment (LI) mice to investigate the interaction between PDE4 and DISC vivo vitro. [11C](R)-Rolipram binding measured by PET LI (n = 11) C57BL/6 wild-type (WT, n 9) mice. total distribution volumes (VT) were calculated corrected for plasma-free fraction (fP) separate group 6) WT 7) enzyme activity using vitro samples...

10.1177/0271678x18758997 article EN Journal of Cerebral Blood Flow & Metabolism 2018-02-12

Abstract Sensorimotor information processing that underlies normal cognitive and behavioral traits is dysregulated across a subset of neurological psychiatric disorders. The cross-disease deficit in sensorimotor gating poses unique opportunity to integrate hierarchical findings at molecular, cellular, through circuitry levels obtain an in-depth mechanistic understanding this process contributes brain physiology pathophysiology beyond categorical segmentation Based on recording with wild-type...

10.1101/497446 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-12-14

ABSTRACT Major mental illnesses such as schizophrenia (SZ) and bipolar disorder (BP) frequently accompany metabolic conditions, but their relationship is still unclear, in particular at the mechanistic level. We implemented an approach of “from population to neuron”, combining population-based epidemiological analysis with neurobiological experiments using cell animal models based on a hypothesis built from study. characterized high-quality data, olfactory neuronal cells biopsied patients SZ...

10.1101/2020.09.13.20183525 preprint EN medRxiv (Cold Spring Harbor Laboratory) 2020-09-14

Summary Reduced BDNF and GABAergic inhibition co-occur in neuropsychiatric diseases, including major depression. Genetic rodent studies show a causal link, suggesting the presence of biological pathways that mediate this co-occurrence. Here we mice with reduced Bdnf ( +/- ) have upregulated expression sequestosome-1/p62, an autophagy-associated stress response protein, surface presentation α5 subunit-containing GABA A receptor (α5-GABA R) prefrontal cortex (PFC) pyramidal neurons. Reducing...

10.1101/334466 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-05-30
Coming Soon ...