Hiroshi Nishimune, PhD

Associate Professor
Anatomy and Cell Biology

Ph.D., 1997 Osaka University, Japan
Postdoctoral, IBDM, INSERM U.382, France, C.E. Henderson lab
Postdoctoral, Washington Univ. Sch. of Med., St. Louis, J.R. Sanes lab
Postdoctoral, Harvard Univ. Dept. MCB, Cambridge, J.R. Sanes lab

Publications: Click here for PubMed, Click here for Google Scholar

The nervous system plays essential roles for our daily life, for example, movement, communicating, sensing, learning, and memory. All these functions of the nervous system depend on cell-cell communication at synapses. We are interested in the molecular mechanisms of synapse formation, maintenance, and how it degenerates in Amyotrophic lateral sclerosis (ALS) and aging.

Motor neuron degeneration in ALS patients and animal models is preceded by neuromuscular junction (NMJ, the synapse between motor neurons and muscles) denervation, which suggests that ALS is a dying-back neuropathy. The mechanisms of NMJ denervation and the reasons for the preferential death of motor neurons in ALS remain unknown; therefore, effective treatments for ALS are lacking. Thus, our long-term goal is to elucidate the molecular mechanisms underlying denervation in ALS to identify new therapeutic targets.

Aged rodents also show NMJ denervation similar to ALS model rodents. We identified that physical exercise ameliorates NMJ denervation and degeneration of synaptic proteins in NMJs of aged rats. We seek exercise activated molecular mechanisms that have beneficial role for the maintenance of NMJs in aged animals.

Presynaptic active zones are synaptic vesicle release sites that play essential roles for synaptic transmission and pathology of NMJs (Figure 1). Our studies show that NMJ active zones are organized via interactions between an active zone-organizer, a receptor for the organizer (presynaptic voltage dependent calcium channels, VDCC), and active zone proteins (Figure 2). However, active zones become impaired during aging and ALS. Propitiously, muscle exercise ameliorates the active zone impairment in aged NMJs, which suggests the potential for therapeutic strategies (Figure 3). Currently, we are applying our knowledge to study the degeneration mechanism of ALS NMJs, and seek ways to ameliorate NMJ denervation in ALS model animals using exercise intervention and adult stem cells.

figure 1

figure 2

Figure 3

Lab Members

Hiroshi Nishimune
S Tungtur
N Nishimune
Hiroshi Nishimune, PhD
Associate Professor
Sudheer Tungtur, MS
Research Associate
 Natsuko Nishimune
Research Assistant
Y Badawi
Robert Rogers Phd  
 Yomna Badawi, PhD
Postdoctoral Fellow
 Robert Rogers, PhD
Postdoctoral Fellow

Former Lab Members

  • Takafumi Mizushige, PhD: Associate Professor Department of Applied Biological Chemistry, Faculty of Agriculture, Utsunomiya University
  • Sara Billings, MS: Research Assistant, Stanford School of Medicine
  • Jie Chen, MD PhD: Kansas City
  • Gwenaelle Clarke, PhD: Private Corporation
  • Lisa Nadeau: Kirksville College of Osteopathic Medicine (2013)
  • Tomohiro Tanaka, PhD: Postdoctoral fellow, Scripps Research Institute


Midwest Stem Cell Therapy Center
2015 ALS Ice Bucket Challenge with Dr. Rick Barohn, Dept Neurology, August 28th 2015
Last modified: Nov 16, 2015

Hiroshi Nishimune


Hiroshi Nishimune, PhD
Associate Professor

3901 Rainbow Blvd.,
MS 3051, HLSIC Rm. 2073
Kansas City, KS 66160, USA

P: 913-588-4146
F: 913-588-5677