Amyloid beta (Aβ or Abeta) is a peptide of 36–43 amino acids that is processed from the Amyloid precursor protein. While best known as a component of amyloid plaques in association with Alzheimer's disease, evidence has been found that Aβ is a highly multifunctional peptide with significant non-pathological activity.[1] Aβ is the main component of deposits found in the brains of patients with Alzheimer's disease
Harrison FE, Allard J, Bixler R, Usoh C, Li L, May JM, McDonald MP : et. al. et.al. et.al
Author of the Paper: Harrison FE, Allard J, Bixler R, Usoh C, Li L, May JM, McDonald MP.
Title of the Paper: Antioxidants and cognitive training interact to affect oxidative stress and memory in APP/PSEN1 mice.
Journals:
Nutr Neurosci. 2009 Oct;12(5):203-18.
Address of correspondence : Department of Pharmacology, Vanderbilt University, Nashville, TN 37232-0475, USA. fiona.harrison@vanderbilt.edu
Abstract of the Paper
The present study investigated the relationships among oxidative stress, beta-amyloid and cognitive abilities in the APP/PSEN1 double-transgenic mouse model of Alzheimer's disease. In two experiments, long-term dietary supplements were given to aged APP/PSEN1 mice containing vitamin C alone (1 g/kg diet; Experiment 1) or in combination with a high (750 IU/kg diet, Experiments 1 and 2) or lower (400 IU/kg diet, Experiment 2) dose of vitamin E. Oxidative stress, measured by F(4)-neuroprostanes or malondialdehyde, was elevated in cortex of control-fed APP/PSEN1 mice and reduced to wild-type levels by vitamin supplementation. High-dose vitamin E with C was less effective at reducing oxidative stress than vitamin C alone or the low vitamin E+C diet combination. The high-dose combination also impaired water maze performance in mice of both genotypes. In Experiment 2, the lower vitamin E+C treatment attenuated spatial memory deficits in APP/PSEN1 mice and improved performance in wild-type mice in the water maze. Amyloid deposition was not reduced by antioxidant supplementation in either experiment.
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