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:
Joseph JA, Shukitt-Hale B, Denisova NA, Prior RL, Cao G, Martin A, Taglialatela G, Bickford PC (1998) Long-term dietary strawberry, spinach, or vitamin E supplementation retards the onset of age-related neuronal signal-transduction and cognitive behavioral deficits. J Neurosci 18, 8047-8055. Abstract.
Joseph JA, Shukitt-Hale B, Denisova NA, Bielinski D, Martin A, McEwen JJ, Bickford PC (1999) Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation. J Neurosci 19, 8114-8121. Abstract.
Nunomura A, Perry G, Aliev G, Hirai K, Takeda A, Balraj EK, Jones PK, Ghanbari H, Wataya T, Shimohama S, Chiba S, Atwood CS, Petersen RB, Smith MA (2001) Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol 60, 759-767. Abstract.
Russell RL, Siedlak SL, Raina AK, Bautista JM, Smith MA, Perry G (1999) Increased neuronal glucose-6-phosphate dehydrogenase and sulfhydryl levels indicate reductive compensation to oxidative stress in Alzheimer disease. Arch Biochem Biophys 370, 236-239. Abstract.
Smith MA, Kutty RK, Richey PL, Yan S-D, Stern D, Chader GJ, Wiggert B, Petersen RB, Perry G (1994) Heme oxygenase-1 is associated with the neurofibrillary pathology of Alzheimer’s disease. Am J Pathol 145, 42-47. Abstract.
Wataya T, Nunomura A, Smith MA, Siedlak SL, Harris PLR, Shimohama S, Szweda LI, Kaminski MA, Avila J, Price DL, Cleveland DW, Sayre LM, Perry G (2002) High molecular weight neurofilament proteins are physiological substrates of adduction by the lipid peroxidation product hydroxynonenal. J Biol Chem 277, 4644-4648. Abstract.
Casadesus G, Shukitt-Hale B, Joseph JA (2002) Qualitative versus quantitative caloric intake: are they equivalent paths to successful aging? Neurobiol Aging, in press.
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