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


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

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