Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models

Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP...

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Published inScientific reports Vol. 11; no. 1; pp. 5736 - 13
Main Authors Tosh, Justin L., Rhymes, Elena R., Mumford, Paige, Whittaker, Heather T., Pulford, Laura J., Noy, Sue J., Cleverley, Karen, Walker, Matthew C., Tybulewicz, Victor L. J., Wykes, Rob C., Fisher, Elizabeth M. C., Wiseman, Frances K.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 11.03.2021
Nature Publishing Group
Nature Portfolio
Subjects
631/208/207
631/208/2490
631/208/366
631/378
631/378/1689
631/378/2583
692/617/375/365
Age
Alzheimer Disease - complications
Alzheimer Disease - genetics
Alzheimer's disease
Amyloid beta-Peptides - chemistry
Amyloid beta-Peptides - genetics
Amyloid beta-Protein Precursor - genetics
Amyloid precursor protein
Animal models
Animals
Brain - pathology
Chromosome 21
Chromosomes
Chromosomes, Mammalian - genetics
Disease Models, Animal
Down syndrome
Down Syndrome - complications
Down Syndrome - genetics
Down's syndrome
Genes
Humanities and Social Sciences
Mice
Mice, Transgenic
multidisciplinary
Neurodegenerative diseases
Phenotype
Phosphotransferases - metabolism
Protein Aggregates
Protein-Arginine N-Methyltransferases - metabolism
Science
Science (multidisciplinary)
Segmental Duplications, Genomic
Seizures - complications
Seizures - pathology
Solubility
Survival Analysis
Transgenes
Trisomy
Online AccessGet full text

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Abstract Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP , influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.
AbstractList Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.
Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP , influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.
Abstract Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.
Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer's disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or 'dose' of APP is thought to be the cause of this early-onset Alzheimer's disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer's disease in people who have Down syndrome.Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer's disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or 'dose' of APP is thought to be the cause of this early-onset Alzheimer's disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer's disease in people who have Down syndrome.
ArticleNumber 5736
Author Mumford, Paige
Whittaker, Heather T.
Pulford, Laura J.
Noy, Sue J.
Rhymes, Elena R.
Fisher, Elizabeth M. C.
Walker, Matthew C.
Tybulewicz, Victor L. J.
Tosh, Justin L.
Cleverley, Karen
Wiseman, Frances K.
Wykes, Rob C.
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Snippet Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β...
Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer's disease, in which amyloid-β...
Abstract Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which...
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SubjectTerms 631/208/207
631/208/2490
631/208/366
631/378
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Age
Alzheimer Disease - complications
Alzheimer Disease - genetics
Alzheimer's disease
Amyloid beta-Peptides - chemistry
Amyloid beta-Peptides - genetics
Amyloid beta-Protein Precursor - genetics
Amyloid precursor protein
Animal models
Animals
Brain - pathology
Chromosome 21
Chromosomes
Chromosomes, Mammalian - genetics
Disease Models, Animal
Down syndrome
Down Syndrome - complications
Down Syndrome - genetics
Down's syndrome
Genes
Humanities and Social Sciences
Mice
Mice, Transgenic
multidisciplinary
Neurodegenerative diseases
Phenotype
Phosphotransferases - metabolism
Protein Aggregates
Protein-Arginine N-Methyltransferases - metabolism
Science
Science (multidisciplinary)
Segmental Duplications, Genomic
Seizures - complications
Seizures - pathology
Solubility
Survival Analysis
Transgenes
Trisomy
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Title Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models
URI https://link.springer.com/article/10.1038/s41598-021-85062-3
https://www.ncbi.nlm.nih.gov/pubmed/33707583
https://www.proquest.com/docview/2500162207
https://www.proquest.com/docview/2552184565
https://www.proquest.com/docview/2501262581
https://pubmed.ncbi.nlm.nih.gov/PMC7952899
https://doaj.org/article/976af835ad394de686b40b465f483f68
Volume 11
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