title: Limited impact of social isolation on Alzheimer-like symptoms in a triple transgenic mouse model.
abstract: Gene-environment interactions are known to play a major role in the ethiopathology of several neuropsychiatric disorders, including Alzheimer's disease (AD). The present study investigates whether environmental manipulations, that is, social isolation, may affect the genetic predisposition to develop AD-related traits in a triple transgenic mouse model (3 x Tg-AD), as suggested by our previous study employing physical exercise (Pietropaolo et al., 2008). Mutant and wild type mice of both sexes were housed singly or in groups from weaning, and evaluated behaviorally at 6 to 7 months of age. Independent of sex, the 3 x Tg-AD genotype was associated with enhanced acoustic startle response, improved performance in the cued version of the water maze and a clear impairment in the Y maze. Notably, the female (but not male) mutant mice showed increased anxiety. Although social isolation was effective in modifying several behaviors, it did not exacerbate any of the AD-like symptoms. Our findings demonstrated the differential susceptibility of the 3 x Tg-AD mouse line to environmental manipulations, showing that social isolation did not induce remarkable effects on the genetically determined AD-like symptoms, in contrast to what previously observed with physical exercise.
authors.affiliation: Laboratory of Behavioral Neurobiology, Swiss Federal Institute of Technology Zurich, Schwerzenbach, Switzerland.
authors.forename: Susanna
authors.initials: S
authors.lastname: Pietropaolo
authors.forename: Yan
authors.initials: Y
authors.lastname: Sun
authors.forename: Ruixi
authors.initials: R
authors.lastname: Li
authors.forename: Corinne
authors.initials: C
authors.lastname: Brana
authors.forename: Joram
authors.initials: J
authors.lastname: Feldon
authors.forename: Benjamin K
authors.initials: BK
authors.lastname: Yee
mesh_terms: D000161:Acoustic Stimulation / Q000379:methods; D000682:Amyloid / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001522:Behavior, Animal; D003463:Cues; D004195:Disease Models, Animal; D004777:Environment; D005106:Exploratory Behavior / Q000502:physiology; D005260:Female; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008568:Memory / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation / Q000235:genetics; D053764:Presenilin-1 / Q000235:genetics; D011571:Psychoacoustics; D013216:Reflex, Startle / Q000235:genetics; D012559:Schizophrenia / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D012934:Social Isolation; D013028:Space Perception / Q000502:physiology; D016875:tau Proteins / Q000235:genetics
chemical_list: D000682:Amyloid; D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1; D016875:tau Proteins