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- W2897524173 abstract "Recent all amyloid treatments failed to recover the cognition, which induced some confusions about a pathogenic mechanism of AD. We try to conclude this confusion by our research findings. Cheril Tapia-Rojas et al's findings and our recent human clinical observation which confirms our previous findings are used for this abstract. Over-feeding of methionine to wild mice induced the typical AD biomarkers such as amyloid beta and phosphorylated-tau. Also over-feeding of methionine induced the oxidative stress, which induced HCA production from methionine and/or homocysteine. HCA in blood induced the cognitive decline of AD patients. Amyloid hypothesis is now calling a question and our this findings indicate that oxidative stress induces amyloid and tau biomarker of AD and also induces HCA which declines the cognition of AD. The biomarker of amyloid does not show directly the cognitive decline and HCA declines the cognition of AD. Amyloid exaggerates HCA toxicity." @default.
- W2897524173 created "2018-10-26" @default.
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- W2897524173 date "2018-07-01" @default.
- W2897524173 modified "2023-10-16" @default.
- W2897524173 title "P4‐237: OXIDATIVE STRESS INDUCES AMYLOID AND TAU ALZHEIMER'S BIOMARKERS AND THE COGNITIVE DECLINE OF ALZHEIMER'S DISEASE BY PRODUCTION OF HOMOCYSTEIC ACID" @default.
- W2897524173 doi "https://doi.org/10.1016/j.jalz.2018.07.058" @default.
- W2897524173 hasPublicationYear "2018" @default.
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