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August 16-17, 2018 | Copenhagen, Denmark
Dementia and Alzheimer ’s Disease
10th World congress on
Journal of Neurology and Neurorehabilitation Research | Volume: 3
Vegetable oil-derived hydroxynonenal causes Alzheimer’s neuronal death via Hsp70.1 depletion
Tetsumori Yamashima
School of Medical Science, Japan
Recent data advocate for dual roles of heat-shock protein
70.1 (Hsp70.1) not only as a molecular chaperone for
altered proteins but also as a guardian of lysosomal integrity.
Thus, in case of Hsp70.1 dysfunction, not only failure of protein
traffic and degradation but also lysosomal destabilization may
occur. In the monkey hippocampal CA1 neurons after transient
ischemia, the author’s group previously found by proteomic
analysis that Hsp70.1 can become an in-vivo target of
carbonylation by a lipid peroxidation product, hydroxynonenal
(HNE). Furthermore, in the in-vitro experiments Hsp70.1
carbonylated by HNE was found to be susceptible to cleavage
by activated μ-calpain. Calpain-mediated Hsp70.1 cleavage
can lead to autophagy failure and lysosomal destabilization
with the resultant release of cathepsins and neuronal death.
Focusing this ‘calpain-cathepsin hypothesis’, I summarize
current advance on ischemic neuronal death, and forward a
perspective view that the causative substance for Alzheimer
neuronal death is actually ‘vegetable oils’. Targeting especially
ω=6 PUFA (poly-unsaturated fatty acid)-derived HNE may
help elucidate the pathogenesis of Alzheimer’s disease.
Speaker Biography
Tetsumori Yamashima is a consultant neurosurgeon specialized in neuroscience.
In 1975, he graduated from Kanazawa University Faculty of Medicine. In 1979, he
completed his research diploma in the Kanazawa University Graduate School Medical
Research Course (Doctor of Medicine). He then studied abroad in Germany and
Sweden, including neuropathology and brain science. He became Chief of Medical
Staff at Kanazawa University Hospital, Associate Professor of Kanazawa University
Medical Faculty, and Director of Restorative Neurosurgery at Kanazawa University
Graduate School of Medical Science. At present, he is CEO of the Arimatsu Medical
and Dental Clinic in Kanazawa city, works at this clinic (Tuesday to Saturday), and at
Minami-gaoka Hospital (consultant neurosurgeon: Monday mornings). At Kanazawa
University Hospital (part-time lecturer: Monday afternoons), he heads a special
“higher brain dysfunction” outpatient clinic. He is acknowledged for using the RBANS
(Repeatable Battery for the Assessment of Neuropsychological Status), MRI and PET
scans for early detection of Alzheimer’s disease, even a few years before dementia
appears, allowing preventive treatment to be carried out. In 1998, he proposed
the “calpain-cathepsin hypothesis” as a mechanism of neuronal cell death. He also
discovered that the causative agent responsible for Alzheimer’s disease is not
amyloid β, but hydroxynonenal derived from “cooking oil”. He is the author of 200
published scientific papers in English, and 75 papers and 15 books in Japanese.
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