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P4‐027: Gene expression profiling of choroid plexus in Alzheimer's disease reveals important implications of CSF dynamics
Author(s) -
Stopa Edward
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.2047
Subject(s) - choroid plexus , gene expression , gene , biology , dementia , pathology , fold change , transcriptome , gene expression profiling , microbiology and biotechnology , cancer research , medicine , disease , endocrinology , genetics , central nervous system
(entorhinal and temporal cortices, and hippocampus) assembled in tissuemicroarray (TMA), immunohistochemistry was performed to examine the expression patterns of Rb in the following groups: 1) asymptomatic AD elderly individuals with AD-related pathology, but no clinical evidence of dementia (Braak IV-VI, CERAD B or C, CDR 0); 2) symptomatic AD elderly individuals with AD-related pathology and dementia (Braak IV-VI, CERAD B or C, CDR 1⁄4 2); and 3) healthy normal individuals (controls) (Braak I-III, CERAD 0 or A, CDR 0). Results: The nuclear staining was low in all groups, although in the group of normal individuals the number of positive nucleus was higher than in the Alzheimer’s groups. However, there also was cytoplasmatic staining with a stronger immunoreactivity in the normal group and a progressive decrease of reactivity in the asymptomatic and symptomatic AD groups, respectively. Conclusions: Our results show a progressive lost of Rb expression in AD patient’s brain, mainly in the cytoplasm. This shift at the subcellular localization of several makers implicated with cell cycle has been shown in AD, but the real biological significance of this change is still unclear. Considering that Rb function as a cell cycle suppressor, this expression lost could facilitate the cell cycle re-entry and neuronal death. In asymptomatic AD individuals, the Rb expression level higher than in symptomatic AD subjects could be helping, together with other mechanisms, the keeping of their normal cognitive function.