title: Caloric restriction attenuates Abeta-deposition in Alzheimer transgenic models.
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.
authors.affiliation: Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089-0191, USA.
authors.forename: Nilay V
authors.initials: NV
authors.lastname: Patel
authors.forename: Marcia N
authors.initials: MN
authors.lastname: Gordon
authors.forename: Karen E
authors.initials: KE
authors.lastname: Connor
authors.forename: Robert A
authors.initials: RA
authors.lastname: Good
authors.forename: Robert W
authors.initials: RW
authors.lastname: Engelman
authors.forename: Jerimiah
authors.initials: J
authors.lastname: Mason
authors.forename: David G
authors.initials: DG
authors.lastname: Morgan
authors.forename: Todd E
authors.initials: TE
authors.lastname: Morgan
authors.forename: Caleb E
authors.initials: CE
authors.lastname: Finch
mesh_terms: D000544:Alzheimer Disease / Q000178:diet therapy* / Q000235:genetics / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology; D031204:Caloric Restriction / Q000379:methods*; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D016874:Neurofibrillary Tangles / Q000378:metabolism; D058225:Plaque, Amyloid / Q000378:metabolism*; D053764:Presenilin-1; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D000097382:CD68 Molecule
chemical_list: D016229:Amyloid beta-Peptides; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D005904:Glial Fibrillary Acidic Protein; D008565:Membrane Proteins; D053764:Presenilin-1; D012333:RNA, Messenger; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C508853:PSEN1 protein, human