Mme Docteur ANCA GAULARD-CORONDAN

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• CABINET DU DR ANCA GAULARD-CORONDAN

  73A FAUBOURG DE MULHOUSE, 68260 Kingersheim

  Libéral
  89 m116 m

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Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Top publications · les plus citées

• 1

  Treatment of Alzheimer's Disease: Beyond Symptomatic Therapies

  International journal of molecular sciences · 2023

  📚 59 citations🎯 RCR 9.47Top 3% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  In an ever-increasing aged world, Alzheimer’s disease (AD) represents the first cause of dementia and one of the first chronic diseases in elderly people. With 55 million people affected, the WHO considers AD to be a disease with public priority. Unfortunately, there are no final cures for this pathology. Treatment strategies are aimed to mitigate symptoms, i.e., acetylcholinesterase inhibitors (AChEI) and the N-Methyl-D-aspartate (NMDA) antagonist Memantine. At present, the best approaches for managing the disease seem to combine pharmacological and non-pharmacological therapies to stimulate cognitive reserve. Over the last twenty years, a number of drugs have been discovered acting on the well-established biological hallmarks of AD, deposition of β-amyloid aggregates and accumulation of hyperphosphorylated tau protein in cells. Although previous efforts disappointed expectations, a new era in treating AD has been working its way recently. The Food and Drug Administration (FDA) gave conditional approval of the first disease-modifying therapy (DMT) for the treatment of AD, aducanumab, a monoclonal antibody (mAb) designed against Aβ plaques and oligomers in 2021, and in January 2023, the FDA granted accelerated approval for a second monoclonal antibody, Lecanemab. This review describes ongoing clinical trials with DMTs and non-pharmacological therapies. We will also present a future scenario based on new biomarkers that can detect AD in preclinical or prodromal stages, identify people at risk of developing AD, and allow an early and curative treatment.

• 2

  Role and Therapeutic Potential for Targeting Fibroblast Growth Factor 10/FGFR1 in Relapsed Rheumatoid Arthritis

  Arthritis & rheumatology (Hoboken, N.J.) · 2024

  📚 31 citations🎯 RCR 5.26Top 7% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  ObjectiveFibroblast‐like synoviocytes (FLSs) contribute to inflammation and joint damage in rheumatoid arthritis (RA). However, the regulatory mechanisms of FLSs in relapse and remission of RA remain unknown. Identifying FLS heterogeneity and their underlying pathogenic roles may lead to discovering novel disease‐modifying antirheumatic drugs.MethodsCombining single‐cell RNA sequencing (scRNA‐seq) and spatial transcriptomics, we sequenced six matched synovial tissue samples from three patients with relapse RA and three patients in remission. We analyzed the differences in the transcriptomes of the FLS subsets between the relapse and remitted phases. We validated several key signaling pathways using quantitative real‐time PCR (qPCR) and multiplex immunohistochemistry (mIHC). We further targeted the critical signals in vitro and in vivo using the collagen‐induced arthritis (CIA) model in rats.ResultsLining and sublining FLS subsets were identified using scRNA‐seq. Differential analyses indicated that the fibroblast growth factor (FGF) pathway was highly activated in the lining FLSs from patients with relapse RA for which mIHC confirmed the increased expression of FGF10. Although the type I interferon pathway was also activated in the lining FLSs, in vitro stimulation experiment suggested that it was independent of the FGF10 pathway. FGF10 knockdown by small interfering RNA in FLSs significantly reduced the expression of receptor activator of NF‐κB ligand. Moreover, recombinant FGF10 protein enhanced bone erosion in the primary human‐derived pannus cell culture, whereas the FGF receptor (FGFR) 1 inhibitor attenuated this process. Finally, administering an FGFR1 inhibitor displayed a therapeutic effect in a CIA rat model.ConclusionThe FGF pathway is a critical signaling pathway in relapse RA. Targeted tissue‐specific inhibition of FGF10/FGFR1 may provide new opportunities to treat patients with relapse RA.

• 3

  The Effectiveness of Tuina in Relieving Pain, Negative Emotions, and Disability in Knee Osteoarthritis: A Randomized Controlled Trial

  Pain medicine (Malden, Mass.) · 2023

  📚 30 citations🎯 RCR 6.74Top 5% NIH🩺 Clinique

  Lire l'abstract Crossref ↓

  AbstractObjectiveTo evaluate the effectiveness of Tuina in relieving the pain, negative emotions, and disability of patients with knee osteoarthritis (KOA).DesignSingle-center, parallel, randomized controlled trial.SettingShanghai Guanghua Integrated Chinese and Western Medicine Hospital, Shanghai, China.SubjectsAdult patients with KOA who were able to speak Chinese and self-report symptoms were eligible.MethodsA total of 104 patients were randomly allocated to receive the 6-week treatment of Tuina (Tuina group) or celecoxib (celecoxib group). Data on pain, negative emotions, and disability were collected at baseline, at week 2, 4, and 6, and follow-up (1 month after the last treatment). The primary outcomes were the pressure pain thresholds. The secondary outcomes were: (1) numerical rating scale at rest and with movement; (2) Hamilton Anxiety Scale; (3) Hamilton Depression Scale; (4) Western Ontario and McMaster Universities Osteoarthritis Index; and (5) clinical effective rate. The adverse events of the trial were evaluated.ResultsIn total, 99 patients completed the follow-up. Generalized linear mixed models were constructed to analyse the between-group differences. Statistically significant differences were found in the interaction effects (P < .05). In evaluating the group effect, statistical differences were found at week 6 and follow-up (P < .05). Further, all variables showed a time effect (P < .05). A statistical difference in the clinical effective rate was found between the Tuina and celecoxib groups (P < .05).ConclusionsTuina produced superior effects for pain, negative emotions, and disability over time, as compared to celecoxib in patients with KOA.

Publications scientifiques (50) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

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