Imperial College London
Alternate

ProfessorVictorTybulewicz

Faculty of Medicine, Department of Immunology and Inflammation

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 3796 1612v.tybulewicz Website CV

 
 
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Location

 

L2-2720Francis Crick InstituteThe Francis Crick Institute

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Summary

 

Publications

Citation

BibTex format

@article{Tosh:2021:10.1038/s41598-021-85062-3,
author = {Tosh, JL and Rhymes, ER and Mumford, P and Whittaker, HT and Pulford, LJ and Noy, SJ and Cleverley, K and LonDownS, Consortium and Walker, MC and Tybulewicz, VLJ and Wykes, RC and Fisher, EMC and Wiseman, FK},
doi = {10.1038/s41598-021-85062-3},
journal = {Scientific Reports},
title = {Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models},
url = {http://dx.doi.org/10.1038/s41598-021-85062-3},
volume = {11},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Tosh,JL
AU  - Rhymes,ER
AU  - Mumford,P
AU  - Whittaker,HT
AU  - Pulford,LJ
AU  - Noy,SJ
AU  - Cleverley,K
AU  - LonDownS,Consortium
AU  - Walker,MC
AU  - Tybulewicz,VLJ
AU  - Wykes,RC
AU  - Fisher,EMC
AU  - Wiseman,FK
DO  - 10.1038/s41598-021-85062-3
PY  - 2021///
SN  - 2045-2322
TI  - Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models
T2  - Scientific Reports
UR  - http://dx.doi.org/10.1038/s41598-021-85062-3
UR  - https://www.ncbi.nlm.nih.gov/pubmed/33707583
UR  - http://hdl.handle.net/10044/1/88295
VL  - 11
ER  -
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