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Updated: Apr 25, 2026

A Technique for Serial Collection of Cerebrospinal Fluid from the Cisterna Magna in Mouse
Published on: November 10, 2008
Age-associated evolution of plasmatic amyloid in mouse lemur primates: relationship with intracellular amyloid
Maggie Roy1, Cécile Cardoso2, Olène Dorieux3
1CEA, DSV, I2BM, MIRCen, URA CEA CNRS 2210, Fontenay aux Roses, France; CNRS, URA 2210, Fontenay aux Roses, France; Research Center on Aging, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
Abstract:
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Amyloid-β peptide (Aβ) deposition in the brain is one of its hallmarks, and the measure of plasma Aβ is considered to be a biomarker for anti-amyloid drug efficacy in animal models of AD. However, age-associated plasmatic Aβ modulation in animal models is practically never addressed in the literature. Mouse lemur primates are used as a model of normal and AD-like cerebral aging. Here, we studied the effect of age on plasmatic Aβ in 58 mouse lemurs aged from 1 to 10 years. A subset of animals presented high plasmatic Aβ, and the proportion of animals with high plasmatic Aβ was higher in aged animals as compared with young ones. Histologic evaluation of the brain of some of these animals was carried out to assess extracellular and intracellular amyloid load. In aged lemurs, plasmatic Aβ was negatively correlated with the density of neurons accumulating deposits of Aβ.
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