Kazuhiro Yamakawa

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Nagoya University

Japan

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Professor Kazuhiro Yamakawa is a faculty member at Nagoya City University in Japan. His research primarily focuses on epilepsy, neuropsychiatric disorders, and the underlying genetic mechanisms associated with these conditions. Recent contributions include studies on the interactions between epilepsy proteins and calcium regulation, as well as large-scale genetic analyses revealing risk loci for drug-resistant epilepsy. His work aims to enhance understanding of cognitive impairment and neurological function.

Recent Grants

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神経発達症におけるSCN2A欠損と環境要因の相互作用の解明

Open Date: 2020-04-01

Close Date: 2023-03-01

Grant: Close

中枢神経系無髄神経の包括的分子機能解析

Open Date: 2017-04-01

Close Date: 2022-03-31

Grant: Close

てんかんの新規発症機構の解明と治療法開発

Open Date: 2013-05-31

Close Date: 2018-03-31

Grant: Close

Munc18-1異常によるてんかん発症メカニズムの解明

Open Date: 2012-01-01

Close Date: 2013-12-31

Grant: Close

Investigation of molecular pathology of Down syndrome by high efficient system

Open Date: 2010-01-01

Close Date: 2012-12-31

Kazuhiro Yamakawa

Research Interests

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About

Recent Grants

Articles (19)

Genome-wide association meta-analyses of drug-resistant epilepsy

Epilepsy protein myoclonin1 interacts with inositol 1,4,5-trisphosphate receptor and reduces calcium ions stored in endoplasmic reticulum

Large-scale animal model study uncovers altered brain pH and lactate levels as a transdiagnostic endophenotype of neuropsychiatric disorders involving cognitive impairment.

Generation and characterization of cerebellar granule neurons specific knockout mice of Golli-MBP.

Exome sequencing of 20,979 individuals with epilepsy reveals shared and distinct ultra-rare genetic risk across disorder subtypes

Neuronal DSCAM regulates the peri-synaptic localization of GLAST in Bergmann glia for functional synapse formation

Suppression of<i>Sleeping Beauty</i>-induced Gliomagenicity in Ts1Cje Mice, a Model of Down Syndrome

Criticality supports cross-frequency cortical-thalamic information transfer during conscious states

GWAS meta-analysis of over 29,000 people with epilepsy identifies 26 risk loci and subtype-specific genetic architecture

Genome-wide identification and phenotypic characterization of seizure-associated copy number variations in 741,075 individuals

Epilepsies of presumed genetic etiology show enrichment of rare variants that occur in the general population

<i>Scn1a</i>-GFP transgenic mouse revealed Nav1.1 expression in neocortical pyramidal tract projection neurons.

Inversed Effects of Nav1.2 Deficiency at Medial Prefrontal Cortex and Ventral Tegmental Area for Prepulse Inhibition in Acoustic Startle Response

A cross-disorder dosage sensitivity map of the human genome

The role of common genetic variation in presumed monogenic epilepsies

CUX2 deficiency causes facilitation of excitatory synaptic transmission onto hippocampus and increased seizure susceptibility to kainate

Distinct gene-set burden patterns underlie common generalized and focal epilepsies

Soticlestat, a novel cholesterol 24‐hydroxylase inhibitor, reduces seizures and premature death in Dravet syndrome mice

Brain-specific heterozygous loss-of-function of ATP2A2, endoplasmic reticulum Ca2+ pump responsible for Darier's disease, causes behavioral abnormalities and a hyper-dopaminergic state.

Collaborators (26)

Heidi Kirsch

Toshitaka Oohashi

Masayuki Itoh

Adam Weitemier

Tsuyoshi Miyakawa

Sarah Weckhuysen

Takao Kohno

Gianpiero Cavalleri

Tohru Yamamoto

Shigeo Okabe

Hiroshi Ageta

Ken-ichi Matsumoto

Paula Marques

Caroline Cusick

Satoko Hattori

Iori Ohmori

Anna Sophia Kirstein

Toshimitsu Suzuki

Kunihiro Tsuchida

Ingrid Scheffer

Samuel Berkovic

Stefan Wolking

Shoko Nishihara

Noritaka Ichinohe

Keizo Takao

Doug Speed

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