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Abstract #0222

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

1 Centre for Advanced Biomedical Imaging, University College London, London, Greater London, United Kingdom, 2 Department of Neurodegenerative Disease, Institute of Neurology, London, Greater London, United Kingdom, 3 MRC 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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