Fructo-oligosaccharide improved brain β-amyloid, β-secretase, cognitive function, and plasma antioxidant levels in D-galactose-treated Balb/cJ mice

Nutr Neurosci. 2017 May;20(4):228-237. doi: 10.1080/1028415X.2015.1110952. Epub 2015 Nov 5.

Abstract

Objectives: Long-term d-galactose injection induces accelerated aging in experimental rodent models. The aim of this study was to determine the effects of dietary fructo-oligosaccharide (FO) on the brain β-amyloid (Aβ), amyloid-associated enzymes, cognitive function, and plasma antioxidant levels in d-galactose-treated Balb/c mice.

Methods: The subcutaneous (s.c.) injection and the dietary treatment were conducted simultaneously for 49 days. Mice (12 weeks of age) were divided into five groups (n = 14/group): control (s.c. saline, control diet) serving as a young control, DG (s.c. 1.2 g d-galactose/kg body weight, control diet), DG + LFO (2.5% w/w FO, low-dose FO diet), DG + HFO (5% w/w FO, high-dose FO diet), and DG + E (α-tocopherol 0.2% w/w, vitamin E diet) as an antioxidant reference group. Another group of older mice (64 weeks of age) without any injection served as a natural aging (NA) group.

Results: The DG and NA groups had greater Aβ levels in the cortex, hippocampus, and the whole brain. High-dose FO, similar to α-tocopherol, attenuated the d-galactose-induced Aβ density in the cortex and hippocampus. In addition, FO attenuated the d-galactose-induced protein expression of Aβ and beta-site amyloid precursor cleaving enzyme of the whole brain in a dose-response manner. Either dose of FO supplementation, similar to α-tocopherol, attenuated the d-galactose-induced cognitive dysfunction. In addition, FO improved the plasma ascorbic acid level in a dose-response manner.

Conclusion: Dietary FO (2.5-5% w/w diet) could attenuate the development of Alzheimer's disease, which was likely to be associated with its systematic antioxidant effects.

Keywords: Alzheimer; Amyloid precursor cleaving enzyme; Fructo-oligosaccharides; d-Galactose; β-Amyloid.

MeSH terms

  • Amyloid Precursor Protein Secretases / genetics
  • Amyloid Precursor Protein Secretases / metabolism*
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Antioxidants / metabolism
  • Ascorbic Acid / blood
  • Brain / drug effects*
  • Brain / metabolism
  • Cognition / drug effects*
  • Cognition Disorders / chemically induced
  • Cognition Disorders / drug therapy*
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Galactose
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Oligosaccharides / pharmacology*
  • alpha-Tocopherol / blood

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • Oligosaccharides
  • fructooligosaccharide
  • Amyloid Precursor Protein Secretases
  • alpha-Tocopherol
  • Ascorbic Acid
  • Galactose