Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Cortical alpha7 nicotinic acetylcholine receptor and beta-amyloid levels in early Alzheimer disease.
Milos D Ikonomovic; Lynn Wecker; Eric E Abrahamson; Joanne Wuu; Scott E Counts; Stephen D Ginsberg; Elliott J Mufson; Steven T Dekosky (Profiled Authors: Mufson, Elliott J; DeKosky, Steven T)
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Archives of neurology 2009;66(5):646-51.
OBJECTIVE: To examine alpha7 nicotinic acetylcholine receptor (nAChR) binding and beta-amyloid (Abeta) peptide load in superior frontal cortex (SFC) across clinical and neuropathological stages of Alzheimer disease (AD). DESIGN: Quantitative measures of alpha7 nAChR by [(3)H]methyllycaconitine binding and Abeta concentration by enzyme-linked immunosorbent assay in SFC were compared across subjects with antemortem clinical classification of no cognitive impairment, mild cognitive impairment, or mild to moderate AD, and with postmortem neuropathological diagnoses. SETTING: Academic medical center. Subjects Twenty-nine elderly retired clergy. MAIN OUTCOME MEASURES: Quantitative measures of alpha7 nAChR binding and Abeta peptide concentration in SFC. RESULTS: Higher concentrations of total Abeta peptide in SFC were associated with clinical diagnosis of mild to moderate AD (P = .02), lower Mini-Mental State Examination scores (P = .003), presence of cortical Abeta plaques (P = .02), and likelihood of AD diagnosis by the National Institute on Aging-Reagan criteria (P = .002). Increased alpha7 nAChR binding was associated with National Institute on Aging-Reagan diagnosis (P = .02) and, albeit weakly, the presence of cortical Abeta plaques (P = .08). There was no correlation between the 2 biochemical measures. CONCLUSIONS: These observations suggest that during the clinical progression from normal cognition to neurodegenerative disease state, total Abeta peptide concentration increases while alpha7 nAChRs remain relatively stable in SFC. Regardless of subjects' clinical status, however, elevated alpha7 nAChR binding is associated with increased Abeta plaque pathology, supporting the hypothesis that cellular expression of these receptors may be upregulated selectively in Abeta plaque-burdened brain areas.
1 Originating Grant
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1.
MUFSON, ELLIOTT JAY
Neurobiology of Mild Cognitive Impairment in the Elderly
1 September 1997 - 31 March 2013
NATIONAL INSTITUTE ON AGING
Total Funding: $ 20,516,366
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
MUFSON, ELLIOTT JAY
Galanin in Alzheimer's Disease
29 September 1991 - 31 May 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 5,750,823
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2.
RAPOPORT, STANLEY I
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,242,387
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3.
MATTSON, MARK
Cellular And Molecular Pathogenesis Of Alzheimer
NATIONAL INSTITUTE ON AGING
Total Funding: $ 2,801,933
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Molecular and cellular neurosciences 2002;20(2):354-65. -
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