Incipient Alzheimer's disease: Microarray correlation analyses reveal major transcriptional and tumor suppressor responses

These findings suggest a new model of Alzheimer's disease pathogenesis in which a genomically orchestrated up-regulation of tumor suppressor-mediated differentiation and involution processes induces the spread of pathology along myelinated axons

Eric M. Blalock; James W. Geddes; Kuey Chu Chen; Nada M. Porter; William R. Markesbery; Philip W. Landfield

2004

Scholarcy highlights

  • Several reasons account for the substantial resistance of Alzheimer's disease pathogenesis to analysis
  • We addressed the problems of high complexity and overlapping criteria by using a strategy combining powerful new gene microarray technology, which permits measurement of the expression of many thousands of genes simultaneously, with statistical correlation analyses
  • In a subsequent step, we identified post hoc those genes within this large set of AD-related gene that correlated with AD markers across a smaller subgroup comprising incipient AD and control subjects
  • Overview of Gene Changes in Incipient AD. These studies reveal that widespread changes in genomic regulation of multiple cellular pathways are major correlates of incipient AD
  • The major transcriptional orchestration seen here in incipient AD may provide a new perspective on the possible origins of these deleterious processes
  • Among up-regulated transcription factor, incipient ADG for tumor suppressor, lipid biosynthesis, and transcriptional repression were more often correlated with neurofibrillary tangle scores

Need more features? Save interactive summary cards to your Scholarcy Library.