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Updated: May 20, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Early increases in soluble amyloid-β levels coincide with cholinergic degeneration in 3xTg-AD mice
M Teresa Girão da Cruz1, Jessica Jordão, Kevin A Dasilva
1Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Biological Sciences, Brain Sciences, Toronto, ON, Canada.
Abstract:
Accumulation of amyloid-β peptides (Aβ) and cholinergic degeneration are hallmarks of Alzheimer's disease (AD). In a triple transgenic mouse model of AD (3xTg-AD), soluble Aβ42 levels were detected in the septum by 2 months of age, reaching their highest levels at 3-6 months and decreasing at 12 months. Deficits in the number of septal cholinergic neurons and the length of hippocampal cholinergic axons were observed starting at 4 months in 3xTg-AD mice. Our results show that septal Aβ and septohippocampal cholinergic pathology in 3xTg-AD mice occur at an early stage of disease.
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