التفاصيل البيبلوغرافية
| العنوان: |
Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology |
| المؤلفون: |
Baglietto-Vargas, David, Forner, Stefania, Cai, Lena, Martini, Alessandra C, Trujillo-Estrada, Laura, Swarup, Vivek, Nguyen, Marie Minh Thu, Do Huynh, Kelly, Javonillo, Dominic I, Tran, Kristine Minh, Phan, Jimmy, Jiang, Shan, Kramár, Enikö A, Nuñez-Diaz, Cristina, Balderrama-Gutierrez, Gabriela, Garcia, Franklin, Childs, Jessica, Rodriguez-Ortiz, Carlos J, Garcia-Leon, Juan Antonio, Kitazawa, Masashi, Shahnawaz, Mohammad, Matheos, Dina P, Ma, Xinyi, Da Cunha, Celia, Walls, Ken C, Ager, Rahasson R, Soto, Claudio, Gutierrez, Antonia, Moreno-Gonzalez, Ines, Mortazavi, Ali, Tenner, Andrea J, MacGregor, Grant R, Wood, Marcelo, Green, Kim N, LaFerla, Frank M |
| المصدر: |
Nature Communications, vol 12, iss 1 |
| بيانات النشر: |
eScholarship, University of California |
| سنة النشر: |
2021 |
| المجموعة: |
University of California: eScholarship |
| مصطلحات موضوعية: |
Biochemistry and Cell Biology, Biological Sciences, Acquired Cognitive Impairment, Neurosciences, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Genetics, Brain Disorders, Aging, Alzheimer's Disease, 2.1 Biological and endogenous factors, Aetiology, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Brain, Disease Models, Animal, Female, Gene Expression Profiling, Gene Ontology, Gene Regulatory Networks, Humans, Male, Mice, Inbred C57BL, Transgenic |
| الوقت: |
2421 |
| الوصف: |
The majority of Alzheimer's disease (AD) cases are late-onset and occur sporadically, however most mouse models of the disease harbor pathogenic mutations, rendering them better representations of familial autosomal-dominant forms of the disease. Here, we generated knock-in mice that express wildtype human Aβ under control of the mouse App locus. Remarkably, changing 3 amino acids in the mouse Aβ sequence to its wild-type human counterpart leads to age-dependent impairments in cognition and synaptic plasticity, brain volumetric changes, inflammatory alterations, the appearance of Periodic Acid-Schiff (PAS) granules and changes in gene expression. In addition, when exon 14 encoding the Aβ sequence was flanked by loxP sites we show that Cre-mediated excision of exon 14 ablates hAβ expression, rescues cognition and reduces the formation of PAS granules. |
| نوع الوثيقة: |
article in journal/newspaper |
| وصف الملف: |
application/pdf |
| اللغة: |
unknown |
| العلاقة: |
qt8589t2jp; https://escholarship.org/uc/item/8589t2jpTest |
| الإتاحة: |
https://escholarship.org/uc/item/8589t2jpTest |
| حقوق: |
public |
| رقم الانضمام: |
edsbas.C6380FCD |
| قاعدة البيانات: |
BASE |
