Blueberries may reduce Alzheimer risk

By Stephen Daniells

- Last updated on GMT

Related tags Oxidative stress Alzheimer's disease Neuron Brain

Eating a diet rich in blueberries may reduce the severity of
neurodegenerative diseases such as Alzheimer's or cognitive
disorders relating to ageing, if results from an animal study can
be translated into humans.

"The current findings would suggest that a diet enriched in blueberry might attenuate degenerative processes due to oxidative or inflammatory stressors similar to the effectiveness of pharmacological strategies related to this hypothesis of Alzheimer's disease,"​ wrote lead author Kara Duffy in the journal Neurobiology of Aging​. Alzheimer's disease is the most common form of dementia and currently affects over 13 million people worldwide. The direct and indirect cost of Alzheimer care is over $100bn (€ 81bn) in the US alone. The direct cost of Alzheimer care in the UK was estimated at £15bn (€ 22bn). This is not the first time that blueberries have been linked to protection from Alzheimer's, with sales of the fruit reported to be booming, going from £10.3m (€14.9m) in 2003 to almost £40m (€58m) in 2005, according to UK supplier BerryWorld. The researchers, from the National Institute on Aging (National Institutes of Health), Tufts University, and Louisiana State University System, randomly assigned Young male Fischer-344 rats a diet containing blueberry extract (two per cent) or a control diet for at least eight weeks. After this the rats were then randomly assigned to receive either a phosphate buffered saline or kainic acid to replicate the neuronal loss experienced by people suffering a neurodegenerative disease. Behavioural studies were then performed and brain functioning was studied to determine any differences in neuronal loss. The researchers reported that the rats that were fed a blueberry supplemented diet had enhanced behavioural performance as measured using performance in a 14-unit T-maze. Duffy and co-workers also report that the blueberry-fed animals experienced significantly less brain cell loss, and had more viable brain cells following oxidative stress. "The present findings indicate that rats exhibited impaired performance in maze learning following intra-hippocampal injection ofkainic acidand that a blueberry enriched diet provided significant protection against these decrements in performance,"​ wrote Duffy. "Additionally… [we] documented clear evidence that the blueberry-enriched diet reduced neuronal loss resulting from the excitotoxic effects ofkainic acid." ​ Although the mechanism of Alzheimers is not clear, more support is gathering for the build-up of plaque from beta-amyloid deposits. The deposits are associated with an increase in brain cell damage and death from oxidative stress. Previous studies have suggested that it is against the oxidative stress that the polyphenols appear to offer protection, although Duffy and co-workers indicate that the benefits of the blueberry extracts may go beyond that of antioxidant. "[Combining our findings] with additional research… suggests that at least part of the efficacy of the blueberry supplementation may be to enhance neuronal signaling in areas of the brain affected bykainic acid. This would allow more effective intra- and inter-area communication and ultimately facilitate both cognitive and motor function,"​ wrote the authors. While further research is required in the area, these results suggest that the wonder fruits rich in antioxidants, such as blueberries, could play a role in the prevention and possible treatment of Alzheimer's disease and other neurodegenerative disorders. Source: Neurobiology of Aging​ (Elsevier) Published on-line ahead of print, doi:10.1016/j.neurobiolaging.2007.04.002 "A blueberry-enriched diet provides cellular protection against oxidative stress and reduces a kainate-induced learning impairment in rats" ​Authors: K.B. Duffy, E.L. Spangler, B.D. Devan, Z. Guo, J.L. Bowker, A.M. Janas, A. Hagepanos, R.K. Minor, R. DeCabo, P.R. Mouton, B. Shukitt-Hale, J.A. Joseph, D.K. Ingram

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