Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease

Smoking exacerbates amyloid pathology in a mouse model of Alzheimer’s disease

“…3). APP/PS1 animals start to develop amyloid plaques around 5-6 months-old 33,34 . At 7 months of age, the control animals and those exposed to a low dose of cigarette smoke, display a small amount of Ab plaques A peristaltic pump was used to suck the smoke from the cigarette and redirect it into the chamber again.…”

“…APPswe/PS1dE9 (B6C3-Tg (APPswe, PSEN1dE9) 85Dbo/J, The Jackson Laboratory) double transgenic mice express a chimeric mouse/human amyloid precursor protein containing the Swedish mutation (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1dE9) gene. The generation and initial characterization of these mice has been reported previously 34 . APP/PS1 animals develop amyloid deposits by 5-6 months old mostly located in the hippocampus, cortex and subiculum and display behavioural impairment by 13 months of age.…”

Activation of Wnt signaling by lithium and rosiglitazone reduced spatial memory impairment and neurodegeneration in brains of an APPswe/PSEN1ΔE9 mouse model of Alzheimer's disease

“…35 These mice and agematched wild types were used to analyze how physiopathological markers of AD were modified by lithium (3 mequiv. kg À1 IP, daily) and rosiglitazone (3 mg kg À1 gavage, daily) treatments initiated at 9 months of age.…”

A GPCR/secretase complex regulates β- and γ-secretase specificity for Aβ production and contributes to AD pathogenesis

“…APP/ PS double-transgenic mice coexpress a chimeric mouse/ human APP Swedish mutant (APPswe) and a mutant human PS1 (PS1ΔE9) [52]. These transgenic mice display an aggressive onset of age-dependent neuritic Aβ deposition in the cortex and hippocampus, and begin to show memory deficits at the age of 6 months [53,54]. Drug administration began prophylactically at 4 months of age (that is, about 2 months before the onset of phenotype).…”