Amyloid-β seeding effects are dependent on the presence of knock-in genes in the AppNL-G-F mice.

Lacoursiere, S. G.; Westaway, D.; Safar, J.; Mohajerani, M. H.; Sutherland, R. J.

doi:10.1101/2022.05.28.492382

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bioRxiv · 10.1101/2022.05.28.492382

Amyloid-β seeding effects are dependent on the presence of knock-in genes in the AppNL-G-F mice.

Lacoursiere, S. G.·Westaway, D.·Safar, J.·Mohajerani, M. H.·Sutherland, R. J.

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Abstract

Alzheimers disease (AD) is characterized by the prion-like propagation of amyloid-{beta} (A{beta}). However, the role of A{beta} in cognitive impairment is still unclear. To determine the causal role of A{beta} in AD, we intracerebrally seeded the entorhinal cortex of two-month-old AppNL-G-F mouse model with an A{beta} peptide derived from patients who died from rapidly progressing AD. When the mice were three and six months of age, or one- and four-months following seeding, respectively, spatial learning and memory were tested using the Morris water task. Immunohistochemical labeling showed seeding with the A{beta} seed increased plaque size one month following seeding, but reduced plaque counts four months following injection compared to the control seeded mice. A significant increase in microgliosis was found. However, we found no correlation between pathology and spatial performance. The results of the present study show that seeding human tissue with or without A{beta} alters learning and memory ability, A{beta} plaque deposition, plaque size, and microgliosis in the AppNL-G-F knock-in model, and these effects are dependent on the presence of a humanized App gene and the presence of A{beta} in the seed. But these pathological changes were not initially causal in memory impairment.

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Lacoursiere, S. G., Westaway, D., Safar, J., Mohajerani, M. H., Sutherland, R. J.. 2022-05-29. Amyloid-β seeding effects are dependent on the presence of knock-in genes in the AppNL-G-F mice.. https://doi.org/10.1101/2022.05.28.492382

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