Caloric restriction attenuates Abeta-deposition in Alzheimer transgenic models

Neurobiol Aging. 2005 Jul;26(7):995-1000. doi: 10.1016/j.neurobiolaging.2004.09.014. Epub 2004 Nov 25.

Abstract

Dietary influences on Alzheimer disease (AD) are gaining recognition. Because many aging processes are attenuated in laboratory mammals by caloric restriction (CR), we examined the effects of short-term CR in two AD-transgenic mice, APP(swe/ind) (J20) and APP(swe) + PS1(M146L) (APP + PS1). CR substantially decreased the accumulation of Abeta-plaques in both lines: by 40% in APP(swe/ind) (CR, 6 weeks), and by 55% in APP + PS1 (CR, 14 weeks). CR also decreased astrocytic activation (GFAP immunoreactivity). These influences of CR on AD-transgenic mice are consistent with epidemiological reports that show that high caloric diets associate with the risk of AD, and suggest that dietary interventions in adult life might slow disease progression.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / diet therapy*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Brain / metabolism
  • Brain / pathology
  • Caloric Restriction / methods*
  • Disease Models, Animal
  • Glial Fibrillary Acidic Protein / metabolism
  • Humans
  • Immunohistochemistry / methods
  • Membrane Proteins / genetics
  • Mice
  • Mice, Transgenic
  • Neurofibrillary Tangles / metabolism
  • Plaque, Amyloid / metabolism*
  • Presenilin-1
  • RNA, Messenger / biosynthesis
  • Reverse Transcriptase Polymerase Chain Reaction / methods

Substances

  • Amyloid beta-Peptides
  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD68 antigen, human
  • Glial Fibrillary Acidic Protein
  • Membrane Proteins
  • PSEN1 protein, human
  • Presenilin-1
  • RNA, Messenger