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.
Disturbed choline plasmalogen and phospholipid fatty acid concentrations in Alzheimer's disease prefrontal cortex.
Miki Igarashi; Kaizong Ma; Fei Gao; Hyung-Wook Kim; Stanley I Rapoport; Jagadeesh S Rao (Profiled Author: Rapoport, Stanley I)
Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. miki.i@uci.edu
Journal of Alzheimer's disease : JAD 2011;24(3):507-17.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by brain deposition of senile (neuritic) plaques containing amyloid-β, neurofibrillary tangles, synaptic loss, neuroinflammation, and overexpression of arachidonic acid (AA, 20:4n-6) metabolizing enzymes. Lipid concentration changes have been reported in different brain regions, but often partially or as a percent of the total concentration. In this study, we measured absolute concentrations (per gram wet weight) of a wide range of lipids in postmortem prefrontal cortex (Brodmann area 9) from 10 AD patients and 9 non-AD controls. Mean total brain lipid, phospholipid, cholesterol, and triglyceride concentrations did not differ significantly between AD and controls. There was a significant 73% decrease in plasmalogen choline, but no difference in other measured phospholipids. Fatty acid concentrations in total phospholipid did not differ from control. However, docosahexaenoic acid (DHA, 22:6n-3) was reduced in ethanolamine glycerophospholipid and choline glycerophospholipid, but increased in phosphatidylinositol. AA was reduced in choline glycerophospholipid, but increased in phosphatidylinositol, while docosatetraenoic acid (22:4n-6), an AA elongation product, was reduced in total brain lipid, cholesteryl ester and triglyceride. These lipid changes, which suggest extensive membrane remodeling, may contribute to membrane instability and synaptic loss in AD and reflect neuroinflammation.
2 Originating Grant
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1.
RAPOPORT, STANLEY I
Brain Imaging In Human Aging, Alzheimer Disease And Other Disorders
NATIONAL INSTITUTE ON AGING
Total Funding: $ 159,786
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2.
RAPOPORT, STANLEY I
Brain Imaging In Human Aging, Alzheimer Disease And Other Disorders
NATIONAL INSTITUTE ON AGING
Total Funding: $ 561,942
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.
RAPOPORT, STANLEY I
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,242,387
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2.
Mayeux, Richard P
GENETIC EPIDEMIOLOGY OF ALZHEIMERS DISEASE IN HISPANICS
1 December 1998 - 31 January 2004
NATIONAL INSTITUTE ON AGING
Total Funding: $ 5,549,515
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3.
Smith, Mark A
METABOLIC ABNORMALITIES IN ALZHEIMER DISEASE
1 May 1999 - 30 April 2006
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 750,386
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2005Khalid Iqbal; Michael Flory; Sabiha Khatoon; Hilkka Soininen; Tuula Pirttila; Maarit Lehtovirta; Irina Alafuzoff; Kaj Blennow; Niels Andreasen; Eugeen Vanmechelen; et al.
Subgroups of Alzheimer's disease based on cerebrospinal fluid molecular markers.
Annals of neurology 2005;58(5):748-57. -
3.
2005Deng-Shun Wang; Richard B Lipton; Mindy J Katz; Peter Davies; Herman Buschke; Gail Kuslansky; Joe Verghese; Steven G Younkin; Chris Eckman; Dennis W Dickson
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Journal of neuropathology and experimental neurology 2005;64(5):378-85.
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