Amyloid precursor protein processing and A 42 deposition in a transgenic mouse model of Alzheimer disease-Reference-Cited by-同舟云学术

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Amyloid precursor protein processing and A 42 deposition in a transgenic mouse model of Alzheimer disease

Published:1997-02-18 Issue:4 Volume:94 Page:1550-1555
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Johnson-Wood K.,Lee M.,Motter R.,Hu K.,Gordon G.,Barbour R.,Khan K.,Gordon M.,Tan H.,Games D.,Lieberburg I.,Schenk D.,Seubert P.,McConlogue L.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference24 articles.

1. Normal and Abnormal Biology of the beta-Amyloid Precursor Protein

2. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease

3. Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene

4. A mutation in the Amyloid Precursor Protein Associated with Hereditary Alzheimer's Disease

5. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid

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4. A Chronic Increase in Blood-Brain Barrier Permeability Facilitates Intraneuronal Deposition of Exogenous Bloodborne Amyloid-Beta1–42 Peptide in the Brain and Leads to Alzheimer’s Disease-Relevant Cognitive Changes in a Mouse Model;Journal of Alzheimer's Disease;2024-03-05

5. Early modulation of the gut microbiome by female sex hormones alters amyloid pathology and microglial function;Scientific Reports;2024-01-21

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