Apple juice concentrate maintains acetylcholine levels following dietary compromise

Article type: Research Article

Authors: Chan, Amy | Graves, Valerie | Shea, Thomas B.^{; *}

Affiliations: Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA

Correspondence: [*] Corresponding auhtor. Tel.: +1 978 934 2881; Fax: +1 978 934 3044; E-mail: [email protected].

Abstract: Oxidative stress contributes to age-related cognitive decline. In some instances, consumption of fruits and vegetables rich in antioxidant can provide superior protection than supplementation with purified antioxidants. Our prior studies have shown that supplementation with apple juice concentrate (AJC) alleviates oxidative damage and cognitive decline in adult (9–12 months) mice lacking ApoE (as a model of increased oxidative stress) and in normal aged (2–2.5 years) mice when challenged with a vitamin-deficient, oxidative stress-promoting diet. Here, we demonstrate that AJC, administered in drinking water, maintains acetylcholine levels that otherwise decline when adult and aged mice are maintained on the above deficient diet. Normal mice aged either 9–10 months or 2–2.5 years and ApoE-/- mice aged 9–10 months were maintained for 1 month on a complete diet or a diet lacking folate and vitamin E and containing iron as a pro-oxidant, and additional groups received 0.5% AJC ad libitum in drinking water. Spectrophotometric assay of acetylcholine levels revealed a significant decline in homogenates of combined frontal cortex and hippocampus for all mice maintained on the deficient diet, and a prevention of this decline in mice maintained on the deficient diet when supplemented with AJC. These findings provide a likely mechanism by which consumption of antioxidant-rich foods such as apples can prevent the decline in cognitive performance that accompanies dietary and genetic deficiencies and aging.

DOI: 10.3233/JAD-2006-9308

Journal: Journal of Alzheimer's Disease, vol. 9, no. 3, pp. 287-291, 2006