We investigated the effects of genetic down- and up-regulation of sac1 expression on Aß42 accumulation and the associated neural deficits in flies with direct expression of arctic mutant Aß42 (Aßarc) in the neurons of GF pathway.
We genetically down-regulated and up-regulated the level of sac1, encoding a major phosphoinositide phosphatases in a disease model, in which arctic mutant Aß42 is directly expressed in the neurons of a neural pathway of adult fruit flies.
We conducted a time-course analysis of Aß42 level in the model and found an age-dependent elevation of Aß42 accumulation, closely correlated to the age-dependent decline of climbing ability in the model flies. Neither sac1 insufficiency nor sac1 over-expression significantly changed the three phenotypes.
We found that the alterations of sac1 expression did not change Aß42 accumulation and neural deficits in the model.