ArticleBMC neurology2019
Inflammatory profiling of patients with familial amyloid polyneuropathy.
Article in BMC neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
- Lower mitochondrial DNA copy number in ATTRV50M Swedish carriers.Orphanet journal of rare diseases · 2026Article
- Disrupted glutathione homeostasis in the pathogenesis of TTR-V30M amyloidosis.Biomarker research · 2026Article
- Application of Omics Analysis in the Clinical Practice and Research of Transthyretin Amyloidosis.Genes · 2026Review
- Oligomeric cystatin C supports the immunosuppressive activity of myeloid cells through interaction with inhibitory receptors.Signal transduction and targeted therapy · 2025Article
- Plasma Proteome Profiling Reveals Inflammation Markers and Tafamidis Effects in V30M Transthyretin Polyneuropathy.International journal of molecular sciences · 2025Article
- Associations between pathophysiological traits and symptom development in retrospective analysis of V30M and V122I transthyretin amyloidosis.International journal of cardiology. Heart & vasculature · 2025Article
- Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach.Communications biology · 2024Article
- Effect of dynamic exclusion and the use of FAIMS, DIA and MALDI-mass spectrometry imaging with ion mobility on amyloid protein identification.Clinical proteomics · 2024Article
- Nerve pathology of microangiopathy and thromboinflammation in hereditary transthyretin amyloidosis.Annals of clinical and translational neurology · 2024Article
- Optimal practices for the management of hereditary transthyretin amyloidosis: real-world experience from Japan, Brazil, and Portugal.Orphanet journal of rare diseases · 2023Review
- Review
- Inflammation across the spectrum of hypertrophic cardiac phenotypes.Heart failure reviews · 2023Review
- Corneal confocal microscopy identifies corneal nerve loss and increased Langerhans cells in presymptomatic carriers and patients with hereditary transthyretin amyloidosis.Journal of neurology · 2023Article
- Tafamidis polyneuropathy amelioration requires modest increases in transthyretin stability even though increases in plasma native TTR and decreases in non-native TTR do not predict response.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2023Article
- Systemic inflammatory markers in patients with polyneuropathies.Frontiers in immunology · 2023Article
- Serum Inflammatory Profile in Hereditary Transthyretin Amyloidosis: Mechanisms and Possible Therapeutic Implications.Brain sciences · 2022Article
- Corneal confocal microscopy to detect early immune-mediated small nerve fibre loss in AL amyloidosis.Annals of clinical and translational neurology · 2022Article
- Transthyretin Amyloid Cardiomyopathy: Impact of Transthyretin Amyloid Deposition in Myocardium on Cardiac Morphology and Function.Journal of personalized medicine · 2022Article
- New Advanced Imaging Parameters and Biomarkers-A Step Forward in the Diagnosis and Prognosis of TTR Cardiomyopathy.Journal of clinical medicine · 2022Review
- Proteostasis Perturbations and Their Roles in Causing Sterile Inflammation and Autoinflammatory Diseases.Cells · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFamilial amyloid polyneuropathy (FAP) or ATTRv (amyloid TTR variant) amyloidosis is a fatal hereditary disease characterized by the deposition of amyloid fibrils composed of transthyretin (TTR). The current diagnosis of ATTRv relies on genetic identification of TTR mutations and on Congo Red-positive amyloid deposits, which are absent in most ATTRv patients that are asymptomatic or early symptomatic, supporting the need for novel biomarkers to identify patients in earlier disease phases allowing disease control.
methodsIn an effort to search for new markers for ATTRv, our group searched for nine inflammation markers in ATTRv serum from a cohort of 28 Brazilian ATTRv patients.
resultsWe found that the levels of six markers were increased (TNF-α, IL-1β, IL-8, IL-33, IFN-β and IL-10), one had decreased levels (IL-12) and two of them were unchanged (IL-6 and cortisol). Interestingly, asymptomatic patients already presented high levels of IL-33, IL-1β and IL-10, suggesting that inflammation may take place before fibril deposition.
conclusionsOur findings shed light on a new, previously unidentified aspect of ATTRv, which might help define new criteria for disease management, as well as provide additional understanding of ATTRv aggressiveness.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.