Literature DB >> 15313836

Loss of apolipoprotein E receptor LR11 in Alzheimer disease.

Clemens R Scherzer1, Katrin Offe, Marla Gearing, Howard D Rees, Guofu Fang, Craig J Heilman, Chica Schaller, Hideaki Bujo, Allan I Levey, James J Lah.   

Abstract

BACKGROUND: Genetic, epidemiologic, and biochemical evidence suggests that apolipoprotein E, low-density lipoprotein receptors, and lipid metabolism play important roles in sporadic Alzheimer disease (AD).
OBJECTIVE: To identify novel candidate genes associated with sporadic AD.
DESIGN: We performed an unbiased microarray screen for genes differentially expressed in lymphoblasts of patients with sporadic AD and prioritized 1 gene product for further characterization in AD brain.
SETTING: Emory University, Atlanta, Ga.
SUBJECTS: Cell lines were used from 14 patients with AD and 9 normal human control subjects.
RESULTS: Six genes were differentially expressed in lymphoblasts of 2 independent groups of patients with probable AD and autopsy-proven AD. We hypothesized that 1 of the genes, termed low-density lipoprotein receptor relative with 11 binding repeats (LR11) (reduced 1.8- and 2.5-fold in AD lymphoblasts vs controls), might be associated with sporadic AD on the basis of its function as neuronal apolipoprotein E receptor. We found dramatic and consistent loss of immunocytochemical staining for LR11 in histologically normal-appearing neurons in AD brains. This reduction of LR11 protein was confirmed by quantitative Western blotting (P =.01).
CONCLUSIONS: There is loss of the microarray-derived candidate, LR11, in neurons of AD brains. This study shows that microarray analysis of widely available lymphoblasts derived from patients with AD holds promise as a primary screen for candidate genes associated with AD.

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Year:  2004        PMID: 15313836     DOI: 10.1001/archneur.61.8.1200

Source DB:  PubMed          Journal:  Arch Neurol        ISSN: 0003-9942


  145 in total

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