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Loss of amyloid precursor protein in a mouse model of Niemann-Pick type C disease exacerbates its phenotype and disrupts tau homeostasis
Ana Nunes
, Sarah N.R. Pressey
,
Jonathan D. Cooper
, Salvador Soriano
Roy and Diana Vagelos Division of Biology & Biomedical Sciences (DBBS)
Bursky Center for Human Immunology & Immunotherapy Programs (CHiiPs)
Division of Genetics and Genomic Medicine
DBBS - Neurosciences
DBBS - Developmental, Regenerative and Stem Cell Biology
DBBS - Molecular Genetics and Genomics
Research output
:
Contribution to journal
›
Article
›
peer-review
23
Scopus citations
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Dive into the research topics of 'Loss of amyloid precursor protein in a mouse model of Niemann-Pick type C disease exacerbates its phenotype and disrupts tau homeostasis'. Together they form a unique fingerprint.
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Keyphrases
Mouse Model
100%
Amyloid Precursor Protein
100%
Homeostasis
100%
NP-C
100%
Dysregulation
50%
Cholesterol
50%
Disease Phenotype
50%
Tau Pathology
25%
Neurodegeneration
25%
Cellular Level
25%
Lysosomal Storage Disease
25%
Astrocytosis
25%
Expression Level
25%
Cumulative Survival Rate
25%
Amyloid Accumulation
25%
Phosphorylation Pattern
25%
Amyloid A
25%
Neuromuscular Coordination
25%
APP Function
25%
Biochemistry, Genetics and Molecular Biology
Mouse Model
100%
Amyloid Precursor Protein
100%
Homeostasis
100%
Tau
100%
Niemann-Pick Disease
100%
Amyloid Protein
33%
Survival Rate
16%
Immunology and Microbiology
Homeostasis
100%
Mouse Model
100%
Precursor
100%
Survival Rate
25%
Neuroscience
Amyloid Precursor Protein
100%
Amyloid Protein
100%
Neurodegeneration
50%
Neuromuscular
50%