ArticleTranslational psychiatry2013
CSF protein biomarkers predicting longitudinal reduction of CSF β-amyloid42 in cognitively healthy elders.
Article in Translational psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- A systematic review and meta-analysis of metalloproteinases in patients with Alzheimer's disease and mild cognitive impairment.Journal of Alzheimer's disease : JAD · 2026Pooled it
- Shared biological pathways for frailty and cognitive impairment: A systematic review.Ageing research reviews · 2018Pooled it
- Association of cerebrospinal fluid amphiphysin-1 levels with cognition and Alzheimer's disease pathology biomarkers.Frontiers in aging neuroscience · 2026Article
- Opposing role of phagocytic receptors MERTK and AXL in Progranulin deficient FTD.Communications biology · 2025Article
- Associations among Angiotensin-Converting Enzyme, Neuroinflammation, and Cerebrospinal Fluid Biomarkers of Alzheimer's Disease in Non-Dementia Adults.Neurotoxicity research · 2025Article
- Critical role of Oas1g and STAT1 pathways in neuroinflammation: insights for Alzheimer's disease therapeutics.Journal of translational medicine · 2025Article
- Charting the Next Road Map for CSF Biomarkers in Alzheimer's Disease and Related Dementias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Serum IL-6, sAXL, and YKL-40 as systemic correlates of reduced brain structure and function in Alzheimer's disease: results from the DELCODE study.Alzheimer's research & therapy · 2023Article
- Multimodal data integration via mediation analysis with high-dimensional exposures and mediators.Human brain mapping · 2022Article
- Concerted type I interferon signaling in microglia and neural cells promotes memory impairment associated with amyloid β plaques.Immunity · 2022Article
- Regulation of microglia phagocytosis and potential involvement of exercise.Frontiers in cellular neuroscience · 2022Review
- Microglia use TAM receptors to detect and engulf amyloid β plaques.Nature immunology · 2021Article
- TAM Signaling in the Nervous System.Brain plasticity (Amsterdam, Netherlands) · 2021Article
- Biomarkers for Alzheimer's Disease Early Diagnosis.Journal of personalized medicine · 2020Review
- Prediction of rapid amyloid and phosphorylated‐Tau accumulation in cognitively healthy individuals.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Dysregulation of TLR5 and TAM Ligands in the Alzheimer's Brain as Contributors to Disease Progression.Molecular neurobiology · 2019Article
- TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration.Disease markers · 2019Review
- Article
- Characterization and clinical use of inflammatory cerebrospinal fluid protein markers in Alzheimer's disease.Alzheimer's research & therapy · 2018Article
- Synaptic proteins in CSF as potential novel biomarkers for prognosis in prodromal Alzheimer's disease.Alzheimer's research & therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
β-amyloid (Aβ) plaque accumulation is a hallmark of Alzheimer's disease (AD). It is believed to start many years prior to symptoms and is reflected by reduced cerebrospinal fluid (CSF) levels of the peptide Aβ1-42 (Aβ42). Here we tested the hypothesis that baseline levels of CSF proteins involved in microglia activity, synaptic function and Aβ metabolism predict the development of Aβ plaques, assessed by longitudinal CSF Aβ42 decrease in cognitively healthy people. Forty-six healthy people with three to four serial CSF samples were included (mean follow-up 3 years, range 2-4 years). There was an overall reduction in Aβ42 from a mean concentration of 211-195 pg ml(-1) after 4 years. Linear mixed-effects models using longitudinal Aβ42 as the response variable, and baseline proteins as explanatory variables (n=69 proteins potentially relevant for Aβ metabolism, microglia or synaptic/neuronal function), identified 10 proteins with significant effects on longitudinal Aβ42. The most significant proteins were angiotensin-converting enzyme (ACE, P=0.009), Chromogranin A (CgA, P=0.009) and Axl receptor tyrosine kinase (AXL, P=0.009). Receiver-operating characteristic analysis identified 11 proteins with significant effects on longitudinal Aβ42 (largely overlapping with the proteins identified by linear mixed-effects models). Several proteins (including ACE, CgA and AXL) were associated with Aβ42 reduction only in subjects with normal baseline Aβ42, and not in subjects with reduced baseline Aβ42. We conclude that baseline CSF proteins related to Aβ metabolism, microglia activity or synapses predict longitudinal Aβ42 reduction in cognitively healthy elders. The finding that some proteins only predict Aβ42 reduction in subjects with normal baseline Aβ42 suggest that they predict future development of the brain Aβ pathology at the earliest stages of AD, prior to widespread development of Aβ plaques.
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