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000136957 0247_ $$2doi$$a10.1016/j.bcp.2012.12.007
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000136957 037__ $$aDZNE-2020-03279
000136957 041__ $$aEnglish
000136957 082__ $$a610
000136957 1001_ $$0P:(DE-HGF)0$$aPopp, Julius$$b0
000136957 245__ $$aCerebral and extracerebral cholesterol metabolism and CSF markers of Alzheimer's disease.
000136957 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2013
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000136957 520__ $$aThe disturbances of the cholesterol synthesis and metabolism described in Alzheimer's disease (AD) may be both a consequence of the neurodegenerative process and a contributor to the pathogenesis. These putative relationships and their underlying mechanisms are not well understood. The aim of this study was to evaluate the relationship between the cerebral and extracerebral cholesterol synthesis and metabolism, and the AD pathology as reflected by CSF markers in humans. We evaluated the relationships between the plasma and the cerebrospinal fluid (CSF) concentrations of cholesterol, the cholesterol precursors lanosterol, lathosterol and desmosterol, and the cholesterol elimination products 24S-hydroxycholesterol and 27-hydroxycholesterol, and the CSF markers for AD pathology Aβ1-42 and p-tau181 in 86 subjects with normal cognition and in 107 AD patients. CSF desmosterol, cholesterol and 24S-hydroxycholesterol in the AD group, and CSF 24S-hydroxycholesterol in the control group correlated with the p-tau181 levels. Neither CSF nor plasma concentrations of the included compounds correlated with the CSF Aβ1-42 levels. In multivariate regression tests including age, gender, albumin ratio, number of the APOEε4 alleles, and diagnosis, p-tau181 levels independently predicted the CSF desmosterol, cholesterol and 24S-hydroxycholesterol concentrations. The associations remained significant for CSF cholesterol and 24S-hydroxycholesterol when analyses were separately performed in the AD group. The results suggest that alterations of CNS cholesterol de novo genesis and metabolism are related to neurodegeneration and in particular to the cerebral accumulation of phosphorylated tau.
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000136957 650_7 $$2NLM Chemicals$$aAmyloid
000136957 650_7 $$2NLM Chemicals$$aBiomarkers
000136957 650_7 $$2NLM Chemicals$$atau Proteins
000136957 650_7 $$097C5T2UQ7J$$2NLM Chemicals$$aCholesterol
000136957 650_2 $$2MeSH$$aAged
000136957 650_2 $$2MeSH$$aAlzheimer Disease: blood
000136957 650_2 $$2MeSH$$aAlzheimer Disease: cerebrospinal fluid
000136957 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000136957 650_2 $$2MeSH$$aAmyloid: metabolism
000136957 650_2 $$2MeSH$$aBiomarkers: blood
000136957 650_2 $$2MeSH$$aBiomarkers: cerebrospinal fluid
000136957 650_2 $$2MeSH$$aBrain: metabolism
000136957 650_2 $$2MeSH$$aCase-Control Studies
000136957 650_2 $$2MeSH$$aCholesterol: metabolism
000136957 650_2 $$2MeSH$$aFemale
000136957 650_2 $$2MeSH$$aHumans
000136957 650_2 $$2MeSH$$aMale
000136957 650_2 $$2MeSH$$atau Proteins: metabolism
000136957 7001_ $$0P:(DE-HGF)0$$aMeichsner, Sabrina$$b1
000136957 7001_ $$0P:(DE-HGF)0$$aKölsch, Heike$$b2
000136957 7001_ $$0P:(DE-HGF)0$$aLewczuk, Piotr$$b3
000136957 7001_ $$0P:(DE-2719)2000015$$aMaier, Wolfgang$$b4$$udzne
000136957 7001_ $$0P:(DE-HGF)0$$aKornhuber, Johannes$$b5
000136957 7001_ $$0P:(DE-2719)2000032$$aJessen, Frank$$b6$$udzne
000136957 7001_ $$0P:(DE-HGF)0$$aLütjohann, Dieter$$b7
000136957 77318 $$2Crossref$$3journal-article$$a10.1016/j.bcp.2012.12.007$$b : Elsevier BV, 2013-07-01$$n1$$p37-42$$tBiochemical Pharmacology$$v86$$x0006-2952$$y2013
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