Department of Neuropathology

Research

The final goal of the research of this department is to conquer human neurological disorders including intractable diseases and developmental impediments. Elucidation of the pathogenesis and pathomechanism of the diseases, and establishment of treatments are aimed by multiple operation of research devices, such as immunohistochemical, ultrastructural, biochemical, and molecular biological approaches, in experimental neuropathology based on human neuropathology.

Outline of Projects

  1. Elucidating restitution mechanism and working up therapy for damaged brain and spinal cord in developings and adults.
  2. Pursuing the pathogenesis and pathomechanism of neurodegenerative disorders, particularly amyotrophic lateral sclerosis and parkinsonism-dementia complex.
  3. (Identify) Pathological conformational changes of deposited molecules (tau, synuclein etc) in neurological disorders.
  4. (Specify) Expression and deposition of proteins relevant to neurological disorders.
  5. (Function as an) Interface between molecular biology and neuropathology on human brains.
Figure.
Human spinal cord injury due to dislocation of the 5th (VC5) and 6th (VC6) cervical vertebral bones (arrow). An extensive cavity (syrinx:triangles) is seen far beyond the originally injured portion. We are making every effort to regenerate the nerve tracts by passing axons thorough the cavity in the spinal cord.

Senile plaques and neurofibrillary tangles, principal neuropathological hallmarks for Alzheimer disease, are composed of amyloid beta-protein and tau protein, respectively, both present in normal brains as non-modified soluble form. Their pathological modification leads to formation of fibrils, which deposit intra or extracellularly, as observed also in aging process. Our research is aimed at finding out reasonable therapeutic strategies for Alzheimer disease and related disorders, by clarifying these pathological processes.

Figure.
Senile plaques (blue), neurofibrillary tangles (red) and microglia (green) seen in Alzheimer disease brain. Interactions between these cells and molecules are essential for formation of these lesions.

Staff

OYANAGI Kiyomitsu
KAWAKAMI Emiko
PIAO Yingshan
ANAMIZU Yorito
HASHIMOTO Tomoyo
ISHIHARA Yoshihiro
ITO Umeo
KAMIYA ToshioPhD
KIHIRA Tameko
KUROIWA Toshihiko
MATSUBARA Shiro
MIZUTANI Toshio
MOCHIZUKI Yoko
NAGAO Masahiro
NAKANO Imaharu
OGATA Kentaro
OKAZAWA Hitoshi
SHIMIZU Toshio
SUN Liyuan
WADA Manabu
YAMAZAKI Mineo