ArticleJournal of neural transmission (Vienna, Austria : 1996)2012
Cerebrospinal fluid amyloid-β 2-42 is decreased in Alzheimer's, but not in frontotemporal dementia.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 54 citations in OpenAlex.
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Traumatic Brain Injury and Axonal Damage in the Pathogenesis of Frontotemporal Dementia: A Narrative Review.Cureus · 2026Review
- Chemical signatures delineate heterogeneous amyloid plaque populations across the Alzheimer's disease spectrum.bioRxiv : the preprint server for biology · 2024Article
- Correlative Chemical Imaging Identifies Amyloid Peptide Signatures of Neuritic Plaques and Dystrophy in Human Sporadic Alzheimer's Disease.Brain connectivity · 2023Article
- The Need for Biomarkers in the ALS-FTD Spectrum: A Clinical Point of View on the Role of Proteomics.Proteomes · 2023Review
- Meprin β knockout reduces brain Aβ levels and rescues learning and memory impairments in the APP/lon mouse model for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Article
- Significance of Blood and Cerebrospinal Fluid Biomarkers for Alzheimer's Disease: Sensitivity, Specificity and Potential for Clinical Use.Journal of personalized medicine · 2020Review
- Diagnosis of Alzheimer's disease utilizing amyloid and tau as fluid biomarkers.Experimental & molecular medicine · 2019Review
- Are N- and C-terminally truncated Aβ species key pathological triggers in Alzheimer's disease?The Journal of biological chemistry · 2018Review
- Correction to: Cerebrospinal fluid amyloid-β 2-42 is decreased in Alzheimer's, but not in frontotemporal dementia.Journal of neural transmission (Vienna, Austria : 1996) · 2018Article
- CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios: better diagnostic markers of Alzheimer disease.Annals of clinical and translational neurology · 2016Article
- The Metalloprotease Meprin β Is an Alternative β-Secretase of APP.Frontiers in molecular neuroscience · 2016Review
- Diagnostic value of cerebrospinal fluid Aβ ratios in preclinical Alzheimer's disease.Alzheimer's research & therapy · 2015Article
- Insulin Resistance is Associated with Higher Cerebrospinal Fluid Tau Levels in Asymptomatic APOEɛ4 Carriers.Journal of Alzheimer's disease : JAD · 2015Article
- Cerebrospinal fluid biomarkers of Alzheimer's disease.Neuroscience bulletin · 2014Review
- Meta-Review of CSF Core Biomarkers in Alzheimer's Disease: The State-of-the-Art after the New Revised Diagnostic Criteria.Frontiers in aging neuroscience · 2014Review
- Truncated and modified amyloid-beta species.Alzheimer's research & therapy · 2014Review
- Cerebrospinal fluid biomarkers for differentiation of frontotemporal lobar degeneration from Alzheimer's disease.Frontiers in aging neuroscience · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. For this purpose, 20 non-demented disease controls (NDC), 22 patients with AD and 17 with FTD were comparatively analysed by a novel sequential aminoterminally and carboxyterminally specific immunoprecipitation protocol with subsequent Aβ-SDS-PAGE/immunoblot, allowing the quantification of peptides 1-38(ox), 2-40 and 2-42 along with Aβ 1-37, 1-38, 1-39, 1-40, 1-40(ox) and 1-42. CSF Aβ1-42 was decreased in AD as compared to NDC, but not to FTD. In a subgroup of the patients analyzed, the decrease of Abeta2-42 in AD was evident as compared to both NDC and FTD. Aβ1-38 was decreased in FTD as compared to NDC and AD. For differentiating AD from FTD, Aβ1-42 demonstrated sufficient diagnostic accuracies only when combined with Aβ1-38. Aβ2-42 yielded diagnostic accuracies of over 85 % as a single marker. These accuracy figures could be improved by combining Aβ2-42 to Aβ1-38. Aβ2-42 seems to be a promising biomarker for differentiating AD from other degenerative dementias, such as FTD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.