Abstract
AbstractIt is the first report that the earlier Alzheimer's pathological changes can be induced in normal C57BL mice, by B6 deficient feeding for 3 month, and this pathological changes were completely inhibited by anti-homocysteic acid antibody. According to Koch's postulate, if a pathogen of Alzheimer's disease is administrated to the normal animal, we would observe the Alzheimer's pathology in the normal animal. We actually have observed this pathology in normal C57BL male mice.
Highlights
Our research team has found (1) that anti-homocysteic acid antibody could show the strong cure and preventive effect on 3xTg-AD mice with normal feeding or with vitamin B6 deficient feeding
Our findings show that the pathological process of 3xTg-AD mice was induced by glutamic acid receptor-bound Homocysteic acid (HA)
We show that vitamin B6 deficient feeding in normal C57BL mice whose age was 4 and 9 month-old showed the earlier Alzheimer’s pathological changes such as memory impairment and amyloid accumulation into neurons
Summary
Our research team has found (1) that anti-homocysteic acid antibody could show the strong cure and preventive effect on 3xTg-AD mice with normal feeding or with vitamin B6 deficient feeding. Our findings show that the pathological process of 3xTg-AD mice was induced by glutamic acid receptor-bound HA.
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