Diffuse Cerebral Sclerosis of Schilder

PARIS, FRANCE / ACCESSWIRE / September 12, 2023 / Ad Scientiam, a global leader in digital biomarkers, has announced a partnership with Sanofi to launch MS-DETECT, an international, multicenter, longitudinal study. MS-DETECT aims to evaluate the ability of MSCopilot®, a medical software device, to detect early signs of disability worsening in people with multiple sclerosis (PwMS). The study will draw upon Ad Scientiam's expertise in MS and is financially supported by Sanofi. AdS logo Multiple Sclerosis (MS) is a chronic immune-mediated disease of the central nervous system that affects 2.8 million people worldwide. The disease is characterized by early inflammatory demyelination and subsequent neurodegeneration. Current clinical evaluation of PwMS relies mainly on the Expanded Disability Status Scale (EDSS), which has several limitations. To improve on these assessments, Ad Scientiam has developed MSCopilot®, a software medical device that addresses four dimensions: ambulation/mobility, upper extremity function, cognition, and low-contrast visual acuity. MS-DETECT's main objective is to determine MSCopilot®'s ability to identify subtle and early disability worsening. This will be performed by evaluating MSCopilot® individual and/or composite scores as compared to the Multiple Sclerosis Functional Composite (MSFC) and the EDSS. "MS-DETECT is a pioneering large-scale longitudinal study that explores digital biomarkers for the early detection of disease progression. This study will provide important data to both clinicians and people living with MS," according to Dr. Saad Zinaï, Chief Medical Officer at Ad Scientiam. "Disability worsening in MS has been recently redefined and we now know that this progression can occur independently of relapses. With MS-DETECT, we have an opportunity to develop a digital solution to help detect and monitor the effects of smoldering disease, and evolve treatment goals for MS patients," explains Su-Peing Ng, Global Head of Medical Affairs - Specialty Care at Sanofi. The study also aims to assess the MSCopilot® performance, safety, usability and satisfaction with the solution. "Disease progression can be hard to detect in routine practice. I believe these novel digital biomarkers are key to help clinicians make appropriate treatment decisions and, ultimately, improve patients' care," said Prof. Patrick Vermersch (Lille, France), Coordinating Investigator and Chairman of the Study Steering Committee. The MS-DETECT study will include 314 PwMS and will be conducted in the United States, Canada, Germany, Italy, Spain, Denmark and France. Several investigative sites have already been initiated in North America and Europe and first patients are expected to participate in the study during Q3 2023. Check our LinkedIn, Facebook, Instagram pages or visit adscientiam.com Contact Information Saad Zinaï Chief Medical Officer szinai@adscientiam.com +33768008666 Matthieu Lamy President mlamy@adscientiam.com +33768008666 SOURCE: Ad Scientiam View source version on accesswire.com:

A study in mice suggests that inflammation in the brain's barrier, the meninges, may spill over into grey matter and cause changes that can contribute to progressive multiple sclerosis (MS). A study in mice suggests that inflammation in the brain's barrier, the meninges, may spill over into grey matter and cause changes that can contribute to progressive multiple sclerosis (MS). The research, published today as a Reviewed Preprint in eLife, is described by the editors as an important study that advances our understanding of the mechanisms of brain damage in this autoimmune disease. It involves the use of novel methods to provide what they say is convincing evidence for a gradient of immune genes and inflammatory markers from the meninges to the adjacent brain tissue in mice. Inflammation within the meninges is found in all types of MS. There is mounting evidence to suggest this inflammation plays a pivotal role in the progression of the disease, including loss of the protective coating on nerves (demyelination), loss of new nerve sprouts (neurites) and decreased volume of grey matter. "Grey matter injury is linked to disabling MS symptoms like cognitive dysfunction and depression," explains Sachin Gadani, a neuroimmunology fellow at Johns Hopkins University School of Medicine, Baltimore, US, and a co-first author of the study alongside Saumitra Singh, Postdoctoral Research Fellow at Johns Hopkins University School of Medicine. "Meningeal inflammation appears to be a critical driver of cortical grey matter pathology, but attempts to characterise the mechanism in an unbiased manner have been limited by the absence of spatially resolved data -- that is, critical information about the anatomical relationship between meningeal inflammation and the underlying brain tissue. We set out to determine the patterns of gene activity in the meninges and the surrounding grey matter, while preserving the context about the position of those cells in the brain." Gadani, Singh and colleagues used an approach called spatial transcriptomics, whereby the pattern of gene activity in a tissue is measured and the information is then pieced back together to show the pattern of gene activity in the original location. They started by measuring gene activity in the inflamed meninges in a mouse model of MS against the meninges in healthy mice, and then compared this to the expression of genes in the surrounding grey matter in both groups of mice. As the team expected, they found an increased expression (upregulation) of genes related to immune cells and pathways, immune cell infiltration, and the activation of brain-specific immune cells called microglia. To understand more about the proximity of this gene activity to the meningeal region, they analysed patterns of gene activity along a path from the meninges to the thalamus. All the groups of genes declined in activity with increasing distance from the inflamed meningeal region. However, some genes showed a more gradual decline -- particularly those involved in immune processes such as antigen processing and presentation. This suggests that some upregulation of pro-inflammatory genes had spilled over from the brain's meningeal region into the grey matter. "This is the first time a study has characterised a mouse model of meningeal inflammation and grey matter injury using spatial transcriptomics," says co-first author Saumitra Singh. "We've provided a publicly available dataset from our work that we hope others can use in future research." A limitation of this study is that the spatial resolution may not be sufficient to distinguish between the meninges and surrounding grey matter with certainty. Additionally, while the authors used a mouse model that represents many pathological features of MS, it does not fully represent human disease, and the analysis does not consider different timepoints in the development of MS. Despite this, the authors say their findings could pave the way for future studies using human samples. "Our findings have revealed several candidate pathways in the development of grey matter injury. Future work should focus on spatial transcriptomics in human samples which, thanks to advances in technology, is now becoming more feasible," concludes senior author Pavan Bhargava, Associate Professor of Neurology at Johns Hopkins University School of Medicine.