ArticleActa neuropathologica communications2021
MFG-E8 (LACTADHERIN): a novel marker associated with cerebral amyloid angiopathy.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Rapid elongation drives the exceptionally fast aggregation of the most common localized human amyloid medin.Communications chemistry · 2026Article
- Use of anti-amyloid-β monoclonal antibodies in persons with Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Reviewing the possible connection between cerebral amyloid angiopathy and blood-brain barrier integrity in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Bridging Inflammation and Repair: The Promise of MFG-E8 in Ischemic Stroke Therapy.International journal of molecular sciences · 2025Review
- Disruption of the cerebrospinal fluid-plasma protein balance in cognitive impairment and aging.Nature medicine · 2025Article
- Proteomic analysis of Down syndrome cerebrospinal fluid compared to late-onset and autosomal dominant Alzheimer´s disease.Nature communications · 2025Article
- Medin synergized with vascular amyloid-beta deposits accelerates cognitive decline in Alzheimer's disease: a potential biomarker.Neural regeneration research · 2024Article
- Proximity extension assay in cerebrospinal fluid identifies neurofilament light chain as biomarker of neurodegeneration in sporadic cerebral amyloid angiopathy.Alzheimer's research & therapy · 2024Article
- Potent CTLs can be induced against tumor cells in an environment of lower levels of systemic MFG-E8.Cancer science · 2024Article
- Proteomics of mouse brain endothelium uncovers dysregulation of vesicular transport pathways during aging.Nature aging · 2024Article
- Computational insights into the cross-talk between medin and Aβ: implications for age-related vascular risk factors in Alzheimer's disease.Briefings in bioinformatics · 2024Article
- Fluid biomarkers in cerebral amyloid angiopathy.Frontiers in neuroscience · 2024Review
- Article
- Light, Water, and Melatonin: The Synergistic Regulation of Phase Separation in Dementia.International journal of molecular sciences · 2023Review
- DCI after Aneurysmal Subarachnoid Hemorrhage Is Related to the Expression of MFG-E8.BioMed research international · 2021Article
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Brain accumulation of amyloid-beta (Aβ) is a crucial feature in Alzheimer´s disease (AD) and cerebral amyloid angiopathy (CAA), although the pathophysiological relationship between these diseases remains unclear. Numerous proteins are associated with Aβ deposited in parenchymal plaques and/or cerebral vessels. We hypothesized that the study of these proteins would increase our understanding of the overlap and biological differences between these two pathologies and may yield new diagnostic tools and specific therapeutic targets. We used a laser capture microdissection approach combined with mass spectrometry in the APP23 transgenic mouse model of cerebral-β-amyloidosis to specifically identify vascular Aβ-associated proteins. We focused on one of the main proteins detected in the Aβ-affected cerebrovasculature: MFG-E8 (milk fat globule-EGF factor 8), also known as lactadherin. We first validated the presence of MFG-E8 in mouse and human brains. Immunofluorescence and immunoblotting studies revealed that MFG-E8 brain levels were higher in APP23 mice than in WT mice. Furthermore, MFG-E8 was strongly detected in Aβ-positive vessels in human postmortem CAA brains, whereas MFG-E8 was not present in parenchymal Aβ deposits. Levels of MFG-E8 were additionally analysed in serum and cerebrospinal fluid (CSF) from patients diagnosed with CAA, patients with AD and control subjects. Whereas no differences were found in MFG-E8 serum levels between groups, MFG-E8 concentration was significantly lower in the CSF of CAA patients compared to controls and AD patients. Finally, in human vascular smooth muscle cells MFG-E8 was protective against the toxic effects of the treatment with the Aβ40 peptide containing the Dutch mutation. In summary, our study shows that MFG-E8 is highly associated with CAA pathology and highlights MFG-E8 as a new CSF biomarker that could potentially be used to differentiate cerebrovascular Aβ pathology from parenchymal Aβ deposition.
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