Evatt ML, Delong MR, Khazai N, Rosen A, Triche S, Tangpricha V.
Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease.
Arch Neurol. 2008 Oct;65(10):1348-52.
PubMed.
Our findings in B6-deficient diet are based on the controversial situation of homocysteine risk factor for Alzheimer disease. The New England Journal of Medicine reported that administration of vitamin B6, folic acid and vitamin B12 to older persons did not prevent their cognitive decline, and the author expressed doubt of the homocysteine risk factor. But our B6-deficient condition suggested that homocysteic acid is indeed a real risk factor. B6-deficient food induced a high level of homocysteine, homocysteic sulfonic acid, and homocysteic acid. Then B6-deficient condition is a good means for inducing the homocysteine risk factor in 3xTg-AD mice. Our anti-HA antibody or vaccine treatment did give a strong answer that homocysteic acid is a real risk factor of homocysteine risk and consequently is a real pathogenic factor.
Recently many papers reported that homocysteine induced Aβ40/42, and these phenomena may be related to the homocysteine risk factor for Alzheimer disease. But recent unsatisfactory results of clinical amyloid treatments raised doubt about the amyloid pathogen of Alzheimer disease.
Our findings in B6-deficient conditions give a strong reply that amyloid beta is not related to the homocysteine risk factor and that homocysteic acid is a real homocysteine risk factor.
The manuscript with our findings on anti-HA antibody treatment in 3xTg-AD mice is available at Nature Precedings
Comments
Saga Woman Junior College
Our findings in B6-deficient diet are based on the controversial situation of homocysteine risk factor for Alzheimer disease. The New England Journal of Medicine reported that administration of vitamin B6, folic acid and vitamin B12 to older persons did not prevent their cognitive decline, and the author expressed doubt of the homocysteine risk factor. But our B6-deficient condition suggested that homocysteic acid is indeed a real risk factor. B6-deficient food induced a high level of homocysteine, homocysteic sulfonic acid, and homocysteic acid. Then B6-deficient condition is a good means for inducing the homocysteine risk factor in 3xTg-AD mice. Our anti-HA antibody or vaccine treatment did give a strong answer that homocysteic acid is a real risk factor of homocysteine risk and consequently is a real pathogenic factor.
Recently many papers reported that homocysteine induced Aβ40/42, and these phenomena may be related to the homocysteine risk factor for Alzheimer disease. But recent unsatisfactory results of clinical amyloid treatments raised doubt about the amyloid pathogen of Alzheimer disease.
Our findings in B6-deficient conditions give a strong reply that amyloid beta is not related to the homocysteine risk factor and that homocysteic acid is a real homocysteine risk factor.
The manuscript with our findings on anti-HA antibody treatment in 3xTg-AD mice is available at Nature Precedings
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