. Dietary intake of antioxidants and risk of Alzheimer disease: food for thought. JAMA. 2002 Jun 26;287(24):3261-3. PubMed.

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  1. Interventions to modify oxidant balance to provide protection from Alzheimer disease (AD) are as hotly debated as it has been for other age-related diseases. In recent studies ( Engelhart et al., Foley and White, Morris, et al.), dietary intake of vitamin E and C was associated with a mild lowered risk of AD, yet vitamins supplied by supplements had no benefit. That dietary antioxidants provide protections should be of little surprise given the massive oxidative damage that is a prominent and early feature of AD (Nunomura, et al). However, oxidative phenomena are well-regulated events such that in AD there is a compensatory antioxidant response (Smith, et al., Russel, et al.) and regulatory control of oxidative damage (Wataya, et al). Uni-dimensional antioxidants found in supplements would only perturb this system whereas complex antioxidants found in fruits and vegetables would synergize with endogenous protectants, and may increase neuronal signaling to increase the efficacy of conventional treatments, or may serve to prevent the disease in individuals genetically predisposed to AD (Joseph et al., 1998, 1999; Casadesus et al., 2002). To expect health from a bottle may be too much , but it hopefully heralds a new direction for treatment and prevention.

    George Perry, Gemma Casadesus*, James A. Joseph*, and Mark A. Smith Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio; *USDA-HNRC at Tufts University, 711 Washington Street, Boston, Massachusetts

    References:

    . Long-term dietary strawberry, spinach, or vitamin E supplementation retards the onset of age-related neuronal signal-transduction and cognitive behavioral deficits. J Neurosci. 1998 Oct 1;18(19):8047-55. PubMed.

    . Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation. J Neurosci. 1999 Sep 15;19(18):8114-21. PubMed.

    . Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol. 2001 Aug;60(8):759-67. PubMed.

    . Increased neuronal glucose-6-phosphate dehydrogenase and sulfhydryl levels indicate reductive compensation to oxidative stress in Alzheimer disease. Arch Biochem Biophys. 1999 Oct 15;370(2):236-9. PubMed.

    . Heme oxygenase-1 is associated with the neurofibrillary pathology of Alzheimer's disease. Am J Pathol. 1994 Jul;145(1):42-7. PubMed.

    . High molecular weight neurofilament proteins are physiological substrates of adduction by the lipid peroxidation product hydroxynonenal. J Biol Chem. 2002 Feb 15;277(7):4644-8. PubMed.

    . Qualitative versus quantitative caloric intake: are they equivalent paths to successful aging?. Neurobiol Aging. 2002 Sep-Oct;23(5):747-69. PubMed.

    View all comments by George Perry
  2. As a followup on the subject of 'diet and Alzheimer's disease' please do not miss the following article:

    Brain Cholesterol Pathology is the cause of Alzheimer’s disease [ Full Text ]

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  1. Epidemiology Strengthens Link of Vitamins E and C to Alzheimer’s