While little is known about the mechanisms responsible for the neuronal degeneration seen during Alzheimer’s disease (AD), the progressive, age-related inability of the brain to cope with insults such as oxidative stress may provide a fertile environment for the subsequent development of neurodegenerative disease. In this light, preventative benefits might be achieved through the administration of antioxidant or antiinflammatory agents. In a recent article (Joseph et al., 2003), long-term dietary supplementation with blueberries, a fruit rich in antioxidants, afforded considerable improvements, biochemical as well as behavioral, in the AbPP/PS1 transgenic mouse model of AD. Interestingly, the signaling and behavioral improvements produced by blueberry supplementation in these transgenic animals were not associated with any changes in amyloid-b. This is an exciting...  Read more

While little is known about the mechanisms responsible for the neuronal degeneration seen during Alzheimer’s disease (AD), the progressive, age-related inability of the brain to cope with insults such as oxidative stress may provide a fertile environment for the subsequent development of neurodegenerative disease. In this light, preventative benefits might be achieved through the administration of antioxidant or antiinflammatory agents. In a recent article (Joseph et al., 2003), long-term dietary supplementation with blueberries, a fruit rich in antioxidants, afforded considerable improvements, biochemical as well as behavioral, in the AbPP/PS1 transgenic mouse model of AD. Interestingly, the signaling and behavioral improvements produced by blueberry supplementation in these transgenic animals were not associated with any changes in amyloid-b. This is an exciting finding, since it suggests that cognitive and neuronal changes seen in AD may occur independently of amyloid-b production and deposition. This finding supports challenges to the amyloid-centric view of neurodegeneration (Smith et al., 2002) and suggests that therapeutic efforts targeted towards oxidative stress, or the sources thereof, may provide greater benefit than will the removal of amyloid (Perry et al., 2000). Indeed, previous studies show that diets rich in fruits and vegetables protect our brains from neurodegenerative changes and prevent AD (Smith et al., 1999; Engelhart et al., 2002).

References:
Engelhart MJ, Geerlings MI, Ruitenberg A, van Swieten JC, Hofman A, Witteman JC, Breteler MM. Dietary intake of antioxidants and risk of Alzheimer disease. JAMA. 2002 Jun 26;287(24):3223-9. (Abstract)

Joseph JA, Denisova NA, Arendash G, Gordon M, Diamond D, Shukitt-Hale B, Morgan D. Blueberry supplementation enhances signaling and prevents behavioral deficits in an Alzheimer disease model. Nutr Neurosci. 2003 Jun ;6(3):153-62. (Abstract)

Smith MA, Casadesus G, Joseph JA, Perry G. Amyloid-beta and tau serve antioxidant functions in the aging and Alzheimer brain. Free Radic Biol Med. 2002 Nov 1;33(9):1194-9. (Abstract)

Smith MA, Petot GJ, Perry G. Diet and Oxidative Stress: A Novel Synthesis of Epidemiological Data on Alzheimer's Disease. J Alzheimers Dis. 1999 Nov ;1(4,5):203-206. (Abstract)

Perry G, Nunomura A, Raina AK, Smith MA. Amyloid-beta junkies. Lancet. 2000 Feb 26;355(9205):757. Abstract

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