ArticleScientific reports2016
Rationalising the role of Keratin 9 as a biomarker for Alzheimer's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
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- A differential proteomics study of cerebrospinal fluid from individuals with Niemann-Pick disease, Type C1.Proteomics · 2023Article
- Multi-Omics, an Integrated Approach to Identify Novel Blood Biomarkers of Alzheimer's Disease.Metabolites · 2022Article
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- UV induced changes in proteome of rats plasma are reversed by dermally applied cannabidiol.Scientific reports · 2021Article
- Why Inclusion Matters for Alzheimer's Disease Biomarker Discovery in Plasma.Journal of Alzheimer's disease : JAD · 2021Article
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- Screening for the Proteins That Can Interact with Grouper Nervous Necrosis Virus Capsid Protein.Viruses · 2020Article
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- Amyloid β Induces Early Changes in the Ribosomal Machinery, Cytoskeletal Organization and Oxidative Phosphorylation in Retinal Photoreceptor Cells.Frontiers in molecular neuroscience · 2019Article
- Drug-induced keratin 9 interaction with Hsp70 in bladder cancer cells.Cell stress & chaperones · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Keratin 9 was recently identified as an important component of a biomarker panel which demonstrated a high diagnostic accuracy (87%) for Alzheimer's disease (AD). Understanding how a protein which is predominantly expressed in palmoplantar epidermis is implicated in AD may shed new light on the mechanisms underlying the disease. Here we use immunoassays to examine blood plasma expression patterns of Keratin 9 and its relationship to other AD-associated proteins. We correlate this with the use of an in silico analysis tool VisANT to elucidate possible pathways through which the involvement of Keratin 9 may take place. We identify possible links with Dickkopf-1, a negative regulator of the wnt pathway, and propose that the abnormal expression of Keratin 9 in AD blood and cerebrospinal fluid may be a result of blood brain barrier dysregulation and disruption of the ubiquitin proteasome system. Our findings suggest that dysregulated Keratin 9 expression is a consequence of AD pathology but, as it interacts with a broad range of proteins, it may have other, as yet uncharacterized, downstream effects which could contribute to AD onset and progression.
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Registered trials
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