AI Article Synopsis
- Common mouse models for Alzheimer's often involve overexpressing a human amyloid precursor protein (APP) gene and a mutated presenilin gene.
- Despite having a single APP Swedish mutation, humanized APP knock-in mice (AppNL) do not show typical Alzheimer symptoms like plaque aggregation or cognitive decline.
- Even at 24 months old, AppNL/NL mice show some amyloid-β oligomers, but still lack plaque deposition, reactive gliosis, and cognitive deficits, suggesting a unique aspect of this model.
Article 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-β oligomers in the prefrontal cortex, they do not develop amyloid plaque deposition, reactive gliosis, or cognitive deficits.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218137 | PMC |
| http://dx.doi.org/10.3233/JAD-180410 | DOI Listing |
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