Caloric restriction attenuates Aβ-deposition in Alzheimer transgenic models

• Published in: Neurobiology of aging Vol. 26; no. 7; pp. 995 - 1000
• Main Authors: Patel, Nilay V., Gordon, Marcia N., Connor, Karen E., Good, Robert A., Engelman, Robert W., Mason, Jerimiah, Morgan, David G., Morgan, Todd E., Finch, Caleb E.
• Format: Journal Article
• Language: English
• Published: London Elsevier Inc 01.07.2005; Elsevier Science
• Subjects: AD transgenics; Amyloid deposition; Astrocyte activation; Biological and medical sciences; Caloric restriction; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Medical sciences; Neurology; Amyloid deposition; Astrocyte activation; AD transgenics; Caloric restriction; Nervous system diseases; Alzheimer disease; Neuroglia; Rodentia; Transgenic animal; Astrocyte; Feeding; Cerebral disorder; Vertebrata; Mammalia; Mouse; Central nervous system disease; Degenerative disease; Models; Low calorie diet
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2004.09.014

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 M146 L (APP + PS1). CR substantially decreased the accumulation of Aβ-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.