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Aminoterminally truncated and oxidized amyloid-beta peptide species in Alzheimer's disease
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Reduced CSF carboxyterminally truncated A beta peptides in frontotemporal lobe degenerations
No full textCerebrospinal fluid (CSF) carboxyterminally truncated amyloid-beta (A beta) peptides, A beta 1-42 and tau protein were evaluated in 30 patients with frontotemporal lobe degenerations (FTLD), 30 Alzheimer's disease (AD) patients and 30 non-demented disease controls (NDC) by A beta-SDS-PAGE/immunoblot as well as commercial ELISAs for A beta 1-42 and total tau. FTLD displayed a significant drop of A beta 1-37 (p = 2.7 x 10(-4)), A beta 1-38 (p = 4.2 x 10(-5)) and A beta 1-42 (p = 3.3 x 10(-4)). A beta 1-42 was selectively decreased in AD (p = 8.5 x 10(-1)). Decreased A beta 1-38 enabled contrasts of beyond 85% to distinguish FTLD from AD and NDC patients, alone or in combination. Accordingly, low CSF A beta 1-37 and A beta 1-38 represent a biomarker candidate for FTLD and may reflect disease-specific changes of APP metabolism. Further validation should be carried out on dementias other than AD, diagnostically relevant control groups without dementia and without any evident affection of the central nervous system and subgroups of FTLD. Moreover, independent methods of measurement should be applied to CSF A beta 1-38
Selective reduction of amyloid beta 42 discriminates Alzheimer's disease from Huntington's disease: indication for distinct pathological events in amyloid beta peptide aggregation
No full textNewly identified G-secretase inhibitors block Notch signaling and control multiple myeloma cell profliferation
No full textThe concentrations of amyloid beta 1-42, total Tau and phospho-Tau181 in the CSF of patients with early dementia and MCI as measured with multiplexing technology
No full textTauopathies and synucleinopathies: Do cerebrospinal fluid beta-amyloid peptides reflect disease-specific pathogenesis?
No full textTo evaluate variations in amyloid beta (A beta) peptide pattern in cerebrospinal fluid (CSF) in neurodegenerative disorders. A recently estabfished quantitative urea-based A beta-sodium-dodecylsulfate-polyacrylamide-gel-electrophoresis with western immunoblot (AP-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide (A beta 1-37, 1-38, 1-39, 1-40, 1-42) pattern in CSF. We asked whether the variation might be useful to further elucidate the overlap between or distinctions among neurodegenerative diseases in A beta-processing. We used the A beta-SDS-PAGE/immunoblot to investigate CSF for diseasespecific A beta peptide patterns. CSF samples from 96 patients with mainly clinically diagnosed Alzheimer's disease (n = 15), progressive supranuclear palsy (n = 20), corticobasal degeneration (n =: 12), Parkinson's disease (n = 11), multiple systems atrophy (n = 18), and dementia with Lewy-bodies (n = 20) were analysed as well a comparison group (n = 19). The A beta peptide patterns varied between tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and a-synuctein on Ap-processing
Newly identified G-secretase inhibitors block Notch signaling and control multiple myeloma cell profliferation
No full textCSF diagnosis of Alzheimer's disease and dementia with Lewy bodies
No full textDifferential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is often crucial. CSF Tau protein and Amyloid-beta (A beta) peptides have shown diagnostic value for the diagnosis of AD, but discrimination from DLB was poor. Herein, we investigate CSF of 18 patients with probable AD, 25 with probable DLB and 14 non-demented disease controls (NDC) by A beta-SDS-PAGE/immunoblot and commercially available ELISAs for A beta 1-42 and tau. CSF A beta peptide patterns and tau exhibited disease specific alterations among AD and DLB. The ratio of A beta 1-42 to A beta 1-38 and A beta 1-42 to A beta 1-37, respectively, in combination with absolute tau, yielded a sensitivity and specificity of 100 and 92%, respectively. We conclude that CSF A beta peptide patterns and tau levels reflect disease-specific pathophysiological pathways of these dementias as distinct neurochemical phenotypes. Combined evaluation of these biomarkers provides a reasonable accuracy for differential diagnosis of AD and DLB
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