Abstract:
:We evaluated pathomechanisms and systemic manifestations of Alzheimer disease (AD), an aging-related dementing neurodegenerative disorder, by expression profiling. Blood mononuclear cell (BMC) transcriptomes of sporadic AD subjects and aged-matched normal elderly controls (NEC) were compared using the human NIA microarray. Relative to the NEC samples, the Alzheimer BMC exhibited a significant decline in the expression of genes concerned with cytoskeletal maintenance, cellular trafficking, cellular stress response, redox homeostasis, transcription and DNA repair. We observed decreased expression of several genes which may impact amyloid-beta production and the processing of the microtubule-associated protein tau. The microarray results were validated by quantitative real time PCR and revealed gender differences in the levels of altered gene expression. Our findings attest to the systemic nature of gene dys-regulation in sporadic AD, implicate disruption of cytoskeletal integrity, DNA repair mechanisms and cellular defenses in this condition, and suggest novel pathways of beta-amyloid deposition in this disease. BMC are highly accessible and may reflect molecular events germane to the neuropathophysiology of AD.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Maes OC,Xu S,Yu B,Chertkow HM,Wang E,Schipper HMdoi
10.1016/j.neurobiolaging.2006.08.004subject
Has Abstractpub_date
2007-12-01 00:00:00pages
1795-809issue
12eissn
0197-4580issn
1558-1497pii
S0197-4580(06)00298-3journal_volume
28pub_type
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