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Increased Insoluble Amyloid-? Induces Negligible Cognitive Deficits in Old AppNL/NL Knock-In Mice.


ABSTRACT: Commonly used Alzheimer's disease mouse models are based on the ectopic overexpression of the human amyloid precursor protein (APP) gene, together with a mutant presenilin gene. Surprisingly, humanized APP knock-in mouse models carrying a single APP Swedish mutation (AppNL), failed to develop amyloid plaque aggregation or cognitive deficits. Here we characterized the effect of this mutation in more advanced ages. We show that 24-month-old AppNL/NL mice, despite presenting an age dependent increase in insoluble amyloid-? oligomers in the prefrontal cortex, they do not develop amyloid plaque deposition, reactive gliosis, or cognitive deficits.

SUBMITTER: Salas IH 

PROVIDER: S-EPMC6218137 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Increased Insoluble Amyloid-β Induces Negligible Cognitive Deficits in Old AppNL/NL Knock-In Mice.

Salas Isabel H IH   Callaerts-Vegh Zsuzsanna Z   D'Hooge Rudi R   Saido Takaomi C TC   Dotti Carlos G CG   De Strooper Bart B  

Journal of Alzheimer's disease : JAD 20180101 2


Commonly used Alzheimer's disease mouse models are based on the ectopic overexpression of the human amyloid precursor protein (APP) gene, together with a mutant presenilin gene. Surprisingly, humanized APP knock-in mouse models carrying a single APP Swedish mutation (AppNL), failed to develop amyloid plaque aggregation or cognitive deficits. Here we characterized the effect of this mutation in more advanced ages. We show that 24-month-old AppNL/NL mice, despite presenting an age dependent increa  ...[more]

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