Date:6/2/2010

ther young people can give us a lead on the development of the disease,” said Dr. Conejero-Goldberg. Once they had the human brain tissue and the genotype of the people whose lives were cut short for a variety of reasons they set out to conduct microarray gene expression studies of the tissue itself. Did having an apoE4 genotype have an impact on the genetic expression of the specific tissue and was the tissue that gets destroyed by the illness molecularly different than the tissue that remains healthy until the very end of the illness?
   
The findings of the study were published in Molecular Psychiatry.
   
They found 70 gene transcripts that differed significantly between the two groups, those with APOE4 and those without. And there were regional differences in the expression of APOE4 itself. Some of the genes are known to be involved with pathways that regulate mitochondrial function, calcium regulation and cell-cycle reentry. The differences in the regulation of the genes between the APOE4 carriers and non-APOE4 carriers and the fact that the changes were observed in the tissue hard hit by Alzheimer’s suggests to these scientists that these molecular hits could be working for a lifetime to set in motion a disease in old age that wipes away memories and so much more. On the contrary, changes in the spared brain area may be neuroprotective.
   
“Our findings tell us that something is going on in the brains of at-risk people very early on, decades before the plaques and tangles begin to appear,” said Dr. Conejero-Goldberg, part of the Litwin-Zucker Research Center for the Study of Alzheimer's Disease. Her collaborators outside of the Feinstein include researchers from the National Institute of Mental Health and Albert Einstein College of Medicine.
   
None of the genes that they identified were involved with the classical Alzheime
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