Age-associated evolution of plasmatic amyloid in mouse lemur primates: relationship with intracellular amyloid deposition

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Roy, Maggie | Cardoso, Cécile | Dorieux, Olène | Malgorn, Carole | Epelbaum, Stéphane | Petit, Fanny | Kraska, Audrey | Brouillet, Emmanuel | Delatour, Benoit | Perret, Martine | Aujard, Fabienne | Dhenain, Marc

Edité par CCSD ; Elsevier -

International audience. 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 A β and the proportion of animals with high plasmatic Aβ was higher in aged animals as compared to young ones. Histological evaluation of the brain of some of these animals was carried out to assess extracellular and intracellular amyloid load. In aged lemurs, plasmatic A β was negatively correlated with the density of neurons accumulating deposits of Aβ.

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