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Enlarged early endosomes in the neurons of young Down syndrome (DS) and pre-Alzheimer’s disease (AD) brains suggest that a disturbance in endocytosis is one of the earliest hallmarks of AD pathogenesis in both conditions. We identified a chromosome 21 gene,Intersectin-1(ITSN1) that is up-regulated in DS brains and has a putative function in endocytosis and vesicle trafficking. To elucidate the function ofITSN1and assess its contribution to endocytic defects associated with DS and AD, we generatedItsn1null mice. In knockout mice we found alterations in a number of parameters associated with endocyic and vesicle trafficking events. We found a reduced number of exocytosis events in chromaffin cells and a slowing of endocytosis in neurons. Endosome size was increased in neurons and NGF levels were reduced in the septal region of the brain. Our data is the first indication thatItsn1has a role in endocytosis in anin vivomammalian model, and that a disruption inItsn1expression causes a disturbance in vesicle trafficking and endocytic function in the brain. These results imply a role forITSN1in the early endocytic anomalies reported in DS brains which may have ramifications for the onset of AD.

Mice deficient for the chromosome 21 ortholog Itsn1 exhibit vesicle-trafficking abnormalities