ArticleJournal of neurology2025
Overlapping presence of β-amyloid, tau, p-tau, and α-synuclein in skin nerve fibers in Alzheimer's disease.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Alpha-synuclein structural variants driving tau pathology and disease interaction.Neural regeneration research · 2026Article
- Cell Cycle Dysfunction and Metabolic Alterations Consistent With Pathological Tau in Progressive Supranuclear Palsy Derived Fibroblasts.Molecular neurobiology · 2026Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Exploring the skin as an open window onto neurodegenerative diseases.Translational neurodegeneration · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
objectiveSkin nerve fiber deposition of proteins can be strongly associated with neurodegenerative diseases, such as phosphorylated α-synuclein (p-SN) in synucleinopathies. Little is known about other neurodegenerative proteins, such as tau or β-amyloid, in skin nerve fibers of patients with Alzheimer's disease (AD) and their link to underlying neurodegeneration. We therefore aimed for describing the presence and distribution of these proteins in the skin of patients with AD and non-AD controls.
methodsSkin biopsies were taken from 45 patients with AD (n = 23) and non-AD controls (n = 22). Nerve fibers were identified using antibodies against protein gene product 9.5 (PGP9.5), and protein deposits were evaluated with double-immunostaining of β-amyloid 1-42 (Aβ1-42), p-SN, tau, and phospho-tau (p-tau).
resultsSkin nerve fiber Aβ1-42 was present in 7/23 (30.4%) patients with AD and 7/22 (31.8%) controls. p-tau was detected in 12/23 (52.2%) patients with AD and 9/22 (40.9%) controls. Tau was present in 19/23 (82.6%) patients with AD and 16/22 (72.7%) controls. p-SN was detected in 12/23 (52.2%) patients with AD and 8/22 (36.4%) controls. Frequencies of deposits were not significantly different between groups and protein frequency did not correlate with severity of cognitive impairment.
interpretationDeposits of β-amyloid 1-42, p-SN, tau, and p-tau were detected in skin nerve fibers in both patient groups; however, qualitative assessment did not discriminate between AD and non-AD patients at this sample size. Future analyses of protein distribution and spreading in peripheral nerves may give new insights into the pathophysiology of neurodegenerative diseases, but may require quantitative detection.
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