Nature Communications (Jan 2020)
YAP-dependent necrosis occurs in early stages of Alzheimer’s disease and regulates mouse model pathology
- Hikari Tanaka,
- Hidenori Homma,
- Kyota Fujita,
- Kanoh Kondo,
- Shingo Yamada,
- Xiaocen Jin,
- Masaaki Waragai,
- Gaku Ohtomo,
- Atsushi Iwata,
- Kazuhiko Tagawa,
- Naoki Atsuta,
- Masahisa Katsuno,
- Naoki Tomita,
- Katsutoshi Furukawa,
- Yuko Saito,
- Takashi Saito,
- Ayaka Ichise,
- Shinsuke Shibata,
- Hiroyuki Arai,
- Takaomi Saido,
- Marius Sudol,
- Shin-ichi Muramatsu,
- Hideyuki Okano,
- Elliott J. Mufson,
- Gen Sobue,
- Shigeo Murayama,
- Hitoshi Okazawa
Affiliations
- Hikari Tanaka
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Hidenori Homma
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Kyota Fujita
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Kanoh Kondo
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Shingo Yamada
- Shino-Test Corporation, 2-29-14, Ohino-dai, Minami-ku
- Xiaocen Jin
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Masaaki Waragai
- Department of Neurology, Higashi Matsudo Municipal Hospital
- Gaku Ohtomo
- Department of Neurology, The University of Tokyo, Graduate School of Medicine
- Atsushi Iwata
- Department of Neurology, The University of Tokyo, Graduate School of Medicine
- Kazuhiko Tagawa
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- Naoki Atsuta
- Department of Neurology, Brain and Mind Research Center, Nagoya University Graduate School of Medicine
- Masahisa Katsuno
- Department of Neurology, Brain and Mind Research Center, Nagoya University Graduate School of Medicine
- Naoki Tomita
- Department of Geriatrics & Gerontology, Division of Brain Science, Institute of Development, Aging and Cancer, Tohoku University
- Katsutoshi Furukawa
- Department of Geriatrics & Gerontology, Division of Brain Science, Institute of Development, Aging and Cancer, Tohoku University
- Yuko Saito
- Department of Laboratory Medicine, National Center Hospital, National Center of Neurology and Psychiatry
- Takashi Saito
- Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science
- Ayaka Ichise
- Department of Physiology, Keio University School of Medicine
- Shinsuke Shibata
- Department of Physiology, Keio University School of Medicine
- Hiroyuki Arai
- Department of Geriatrics & Gerontology, Division of Brain Science, Institute of Development, Aging and Cancer, Tohoku University
- Takaomi Saido
- Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science
- Marius Sudol
- Department of Physiology, National University of Singapore, Yong Loo Li School of Medicine
- Shin-ichi Muramatsu
- Department of Neurology, Jichi Medical University
- Hideyuki Okano
- Department of Physiology, Keio University School of Medicine
- Elliott J. Mufson
- Department of Neurobiology and Neurology, Barrow Neurological Institute
- Gen Sobue
- Department of Neurology, Brain and Mind Research Center, Nagoya University Graduate School of Medicine
- Shigeo Murayama
- Department of Neuropathology, Brain Bank for Aging Research, Tokyo Metropolitan Institute of Gerontology
- Hitoshi Okazawa
- Department of Neuropathology, Medical Research Institute and Center for Brain Integration Research, Tokyo Medical and Dental University
- DOI
- https://doi.org/10.1038/s41467-020-14353-6
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 22
Abstract
The precise mechanisms of neuronal cell death in neurodegeneration are not fully understood. Here the authors show that YAP-mediated neuronal necrosis is increased in pre-symptomatic stages of Alzheimer’s disease and intervention to the necrosis rescues extracellular Aβ aggregation and symptoms in a mouse model.
