Cerebral blood flow deficits in the Tc1 mouse model of Downs syndrome
Holly E Holmes 1 , Frances Wiseman 2 , James M O'Callaghan 1 , Jack A Wells 1 , Victor LJ Tybulewicz 3 , Elizabeth MC Fisher 2 , and Mark F Lythgoe 1
Centre for Advanced Biomedical Imaging,
University College London, London, Greater London,
of Neurodegenerative Disease, Institute of Neurology,
London, Greater London, United Kingdom,
National Institute for Medical Research, London, Greater
London, United Kingdom
Down's syndrome (DS) is a genetic condition caused by
the presence of a third copy of chromosome 21.
Individuals with DS have a greater predisposition to
Alzheimer's disease (AD). This is believed to be caused
by the extra dosage of the amyloid precursor protein
(APP) gene: a known AD risk factor which lies on
chromosome 21. AD-like blood flow changes have
previously been observed in clinical DS studies. We
unveil cerebral blood flow changes in the Tc1 mouse
model of DS in the absence of APP. These results suggest
that other genes on chromosome 21 may be contributing to
these AD-like patterns of hypoperfusion.
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