Study findings from Tokyo Medical and Dental University, Department of Neurology provide new insight
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Posted on Nov 22, 2006, 7 a.m.
By Bill Freeman
Investigators publish new data in the report "Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse. Increased oxidative damage is a prominent and early feature in Alzheimer disease (AD). However, whether it is a primary cause or merely a downstream consequence in AD pathology is still unknown," scientists in Tokyo, Japan report.
Investigators publish new data in the report "Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse. Increased oxidative damage is a prominent and early feature in Alzheimer disease (AD). However, whether it is a primary cause or merely a downstream consequence in AD pathology is still unknown," scientists in Tokyo, Japan report.
"We previously generated alpha-tocopherol transfer protein knockout (Ttpa-/-) mice, in which lipid peroxidation in the brain was significantly increased by complete depletion of alpha-tocopherol (alpha-Toc). Here we crossed AD transgenic (APPsw) model mice (Tg2576) with Ttpa-/-mice. The resulting double-mutant (Ttpa-/-APPsw) mice showed earlier and more severe cognitive dysfunction in the Morris water maze, novel-object recognition, and contextual fear conditioning tests. They also showed increased amyloid beta-peptide (Abeta) deposits in the brain by immunohistochemical analysis, which was ameliorated with alpha-Toc supplementation," wrote Y. Nishida and colleagues, Tokyo Medical and Dental University, Department of Neurology.
The researchers concluded: "In this report we provide clear evidence indicating that chronic lipid peroxidation due to alpha-Toc depletion enhances AD phenotype in a mouse model."
Nishida and colleagues published their study in Biochemical and Biophysical Research Communications (Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse. Biochemical and Biophysical Research Communications, 2006;350(3):530-6).
For additional information, contact Y. Nishida, Graduate School, Dept. of Neurology and Neurological Science, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
The publisher's contact information for the journal Biochemical and Biophysical Research Communications is: Academic Press Inc. Elsevier Science, 525 B St., Ste. 1900, San Diego, CA 92101-4495, USA.
Keywords: Japan, Tokyo, Alzheimer Disease, Biochemical, Central Nervous System Disease.
This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2006, Pain & Central Nervous System Week via NewsRx.com.
