What question did this study set out to answer?

To create and characterize a knock-in mouse model expressing wild-type human amyloid-beta under endogenous gene regulation to model sporadic Alzheimer's disease.

April 23, 2021Nature CommunicationsOpen Access

Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology

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Authors

DBDavid Baglietto‐VargasUniversity of California, Irvine SFStefânia FornerUniversity of California, Irvine LCLena Cai

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Implication

Preclinical study demonstrates age-dependent cognitive and synaptic deficits from wild-type human amyloid-beta in mice, suggesting a physiological model for sporadic Alzheimer's disease.

Key Points

To create and characterize a knock-in mouse model expressing wild-type human amyloid-beta under endogenous gene regulation to model sporadic Alzheimer's disease.
Generated knock-in mice by substituting three amino acids in the endogenous mouse App locus to express wild-type human amyloid-beta (hAβ).
Engineered loxP sites flanking exon 14 to permit Cre-mediated conditional deletion of the humanized Aβ sequence.
Assessed age-dependent cognitive performance, synaptic plasticity, brain volume alterations, inflammatory markers, and Periodic Acid-Schiff (PAS) granule accumulation.
Expression of wild-type human Aβ induced age-dependent cognitive impairments, synaptic plasticity deficits, brain volumetric changes, neuroinflammation, and PAS granule accumulation.
Cre-mediated excision of exon 14 completely ablated hAβ expression, reversed cognitive deficits, and decreased the formation of PAS granules.

Cite This Study

Baglietto‐Vargas et al. (2021) studied this question.

synapsesocial.com/papers/6aa427df407158ff5cc7f94c https://doi.org/10.1038/s41467-021-22624-z

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Implication

Preclinical study demonstrates age-dependent cognitive and synaptic deficits from wild-type human amyloid-beta in mice, suggesting a physiological model for sporadic Alzheimer's disease.

Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology

Discussion

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Implication

Key Points

Cite This Study

Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology

Discussion

Member takes

Implication

Key Points

Cite This Study

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