ArticleJournal of neuroinflammation2022
Neuroimmune proteins can differentiate between tauopathies.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 12 citations in OpenAlex.
- Natural Killer Subset Changes and Vascular Endothelial Growth Factor-A Plasma Profile in Progressive Supranuclear Palsy: The NKscape Study.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Meningeal and infiltrating T-cells are associated with repetitive head trauma and tau-mediated neurodegeneration in chronic traumatic encephalopathy.Acta neuropathologica communications · 2026Article
- Proteomic Analysis of Human Chronic Traumatic Encephalopathy Brain Implicates Proteasome and Ribosome Dysfunction in Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Peripheral and central inflammation in progressive supranuclear palsy syndrome: an immunological and imaging neuroinflammation study.Frontiers in immunology · 2026Article
- Proteomic analysis of human chronic traumatic encephalopathy brain implicates proteasome and ribosome dysfunction in disease severity.Molecular neurodegeneration advances · 2026Article
- Diagnostic utility of biomarkers in progressive supranuclear palsy: toward a biotyping framework.Journal of neurology · 2025Review
- Perivascular glial reactivity is a feature of phosphorylated tau lesions in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson's disease models.Journal of neuroinflammation · 2025Article
- Neuroinflammatory mechanisms may help identify candidate biomarkers in chronic traumatic encephalopathy (CTE).Free neuropathology · 2025Review
- Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes.Cell reports · 2024Article
- Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.International journal of molecular sciences · 2024Article
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundTauopathies are a group of neurodegenerative diseases where there is pathologic accumulation of hyperphosphorylated tau protein (ptau). The most common tauopathy is Alzheimer's disease (AD), but chronic traumatic encephalopathy (CTE), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and argyrophilic grain disease (AGD) are significant health risks as well. Currently, it is unclear what specific molecular factors might drive each distinct disease and represent therapeutic targets. Additionally, there is a lack of biomarkers that can differentiate each disease in life. Recent work has suggested that neuroinflammatory changes might be specific among distinct diseases and offers a novel resource for mechanistic targets and biomarker candidates.
methodsTo better examine each tauopathy, a 71 immune-related protein multiplex ELISA panel was utilized to analyze anterior cingulate grey matter from 127 individuals neuropathologically diagnosed with AD, CTE, PSP, CBD, and AGD. A partial least square regression analysis was carried out to perform unbiased clustering and identify proteins that are distinctly correlated with each tauopathy correcting for age and gender. Receiver operator characteristic and binary logistic regression analyses were then used to examine the ability of each candidate protein to distinguish diseases. Validation in postmortem cerebrospinal fluid (CSF) from 15 AD and 14 CTE cases was performed to determine if candidate proteins could act as possible novel biomarkers.
resultsFive clusters of immune proteins were identified and compared to each tauopathy to determine if clusters were specific to distinct disease. Each cluster was found to correlate with either CTE, AD, PSP, CBD, or AGD. When examining which proteins were the strongest driver of each cluster, it was observed the most distinctive protein for CTE was CCL21, AD was FLT3L, and PSP was IL13. Individual proteins that were specific to CBD and AGD were not observed. CCL21 was observed to be elevated in CTE CSF compared to AD cases (p = 0.02), further validating the use as possible biomarkers. Sub-analyses for male only cases confirmed the results were not skewed by gender differences.
conclusionsOverall, these results highlight that different neuroinflammatory responses might underlie unique mechanisms in related neurodegenerative pathologies. Additionally, the use of distinct neuroinflammatory signatures could help differentiate between tauopathies and act as novel biomarker candidate to increase specificity for in-life diagnoses.
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