Correction to: Cerebrospinal fluid amyloid-β 2-42 is decreased in Alzheimer's, but not in frontotemporal dementia.

The respective first and last authors of this article, Mirko Bibl and Jens Wiltfang, would like to clarify the issue of the seeming duplicate publication of a figure in two articles.

Plasma amyloid-beta peptides in acute cerebral ischemia: a pilot study.

Background: Blood-based tests for a rapid and valid diagnosis as well as outcome prognosis of acute stroke are desirable. Recently, plasma Aβ40 was suggested as an independent cerebrovascular risk factor candidate.

Methods: We investigated eight plasma samples of patients with clinical signs of acute cerebral ischemia for derangements of plasma amyloid-beta (Aβ) peptide patterns as compared to 13 patients with other neuropsychiatric diseases.

Characterization of cerebrospinal fluid aminoterminally truncated and oxidized amyloid-β peptides.

Purpose: Carboxyterminally elongated and aminoterminally truncated Aβ peptides as well as their pyroglutamate and oxidized derivates are major constituents of human amyloid plaques. The objective of the present study was to characterize aminoterminally truncated or oxidized Aβ38, Aβ40, and Aβ42 peptide species in immunoprecipitated human cerebrospinal fluid (CSF).

Experimental Design: We invented a novel sequential aminoterminally and carboxyterminally specific immunoprecipitation protocol and used the Aβ-SDS-PAGE/immunoblot for subsequent analysis of CSF Aβ peptide patterns.

Cerebrospinal fluid amyloid-β 2-42 is decreased in Alzheimer's, but not in frontotemporal dementia.

Alzheimer's dementia (AD) and frontotemporal dementias (FTD) are common and their clinical differential diagnosis may be complicated by overlapping symptoms, which is why biomarkers may have an important role to play. Cerebrospinal fluids (CSF) Aβ2-42 and 1-42 have been shown to be similarly decreased in AD, but 1-42 did not display sufficient specificity for exclusion of other dementias from AD. The objective of the present study was to clarify the diagnostic value of Aβ2-42 peptides for the differential diagnosis of AD from FTD.

Aminoterminally truncated and oxidized amyloid-β peptides in the cerebrospinal fluid of Alzheimer's disease patients.

Carboxyterminally elongated and aminoterminally truncated amyloid-β (Aβ) peptides and their oxidized derivates are major constituents of human amyloid plaques. The objective of the present study was to clarify the diagnostic impact of the Aβ peptides 1-38ox, 2-40, and 2-42 peptides on the neurochemical cerebrospinal fluid (CSF) diagnosis of Alzheimer's disease (AD). For this purpose, 22 patients with AD and 20 non-demented disease controls (NDC) were comparatively analyzed for their cerebrospinal fluid pattern of Aβ1-38ox, Aβ2-40, and Aβ2-42 along with Aβ1-37, Aβ1-38, Aβ1-39, Aβ1-40, Aβ1-40ox, and Aβ1-42 using a novel sequential aminoterminally and carboxyterminally specific immunoprecipitation protocol and subsequent analysis in the Aβ-SDS-PAGE/immunoblot.

Stability of amyloid-β peptides in plasma and serum.

Plasma amyloid-β peptide (Aβ) levels have been suggested as a biomarker candidate for detecting incipient AD. Aβ peptides are known to be sensitive to distinct preanalytical sample handling, which calls for standardised preanalytical procedures. We investigated serum and plasma samples of 19 patients with no clinical signs of dementia for different preanalytical sample handlings.

Combined CSF tau, p-tau181 and amyloid-beta 38/40/42 for diagnosing Alzheimer's disease.

Cerebrospinal fluid (CSF) concentrations of amyloid-beta (Abeta) 1-38, 1-40, 1-42, total-tau and phospho-tau in samples from 156 patients with Alzheimer's disease (AD) (n = 44), depressive cognitive complainers (DCC, n = 25) and various other forms of non-Alzheimer dementias (NAD, n = 87) were analyzed by electrochemiluminescence and enzyme linked immunosorbent assay, respectively. A significant decrease of CSF Abeta1-42 was the most powerful single marker for differentiation of AD from DCC, yielding accuracies of beyond 85%. Increased p-tau and the ratio Abeta1-42/Abeta1-38 yielded accuracies of beyond 80 and 85%, respectively, to discriminate AD versus NAD.

CSF amyloid-β 1-38 and 1-42 in FTD and AD: Biomarker performance critically depends on the detergent accessible fraction.

Cerebrospinal fluid (CSF) Aβ1-38, Aβ1-40, and Aβ1-42 were comparatively analyzed by amyloid-beta SDS-PAGE with Western immunoblot (Aβ-SDS-PAGE/immunoblot), electrochemiluminescence detection and ELISA (MSD/ELISA) in patients with Alzheimer's disease (AD, n = 40), frontotemporal dementia (FTD, n = 30), and other dementias (n = 50) and nondemented disease controls (n = 30). CSF Aβ-peptide concentrations were higher and selective decreases of CSF Aβ1-38 in FTD and Aβ1-42 in AD were more evident as measured after SDS-denaturizing of samples by Aβ-SDS-PAGE/immunoblot. The SDS-accessible pool of CSF Aβ1-38 and Aβ1-42, represented by the individual gain of Aβ-peptide yield using Aβ-SDS-PAGE/immunoblot, was reduced in both FTD and AD.

Cerebrospinal fluid neurochemical phenotypes in vascular dementias: original data and mini-review.

Background/aims: The study evaluated the patterns of cerebrospinal fluid (CSF), amyloid-beta (Abeta) peptides, total tau and phospho-tau among Alzheimer's disease (AD) and vascular dementias (VAD).

Methods: Abeta-SDS-PAGE immunoblot and commercially available ELISAs were applied to the CSF analysis of 52 patients with probable (n = 21) and possible (n = 16) VAD, AD with cerebrovascular disease (n = 15), 30 patients with probable AD and 30 nondemented disease controls.

Results: AD and AD with cerebrovascular disease displayed a similar neurochemical phenotype in contrast to nondemented disease controls and probable VAD with regard to tau, p-tau, Abeta1-40(ox) and Abeta1-42%.

Blood-based neurochemical diagnosis of vascular dementia: a pilot study.

Blood-based tests for the differential diagnosis of Alzheimer's disease (AD) are under intensive investigation and have shown promising results with regard to Abeta40 and Abeta42 peptide species in incipient AD. Moreover, plasma Abeta40 was suggested as an independent cerebrovascular risk factor candidate. These considerations prompted us to analyse a total of 72 plasma samples in vascular dementias (VAD, n = 15), AD with cerebrovascular disease (AD with CVD, n = 7), AD (n = 15), Parkinson's disease and Parkinson's disease dementia (PD/PDD, n = 20) and 15 patients with depression that served as controls (DC) for distinct plasma amyloid-beta (Abeta) peptide patterns.