R. Magliozzi
University of Verona Neuroscience, Biomedicine, Movement ScienceSince 2000, in collaboration with Dr. F. Aloisi at Istituto Superiore di Sanità of Roma (Italy), Dr. Magliozzi paid particular attention to the inflammatory response and the role of ectopic lymphoid-like structures in the meningeal compartment of experimental MS animal models. Then in 2004 she started a long period of internship in the UK MS Tissue Bank at Imperial College London (UK) where in 2006 she started the PhD under the supervision of Prof. R. Reynolds and post-mortem MS tissues and in the intrathecal inflammation generated in the cerebrospinal fluid analysis of MS patients. This with the main aim to identify possible neuroimmunological intrathecal mechanisms involved in multiple sclerosis and potential new biomarkers MS progression, as at the moment there are no effective treatment for the progressive stages of the disease. At the Dept of Neuroscience of the University of Verona, she focussed to translate all the results of basic neuroimmunology to the finding of new biomarkers, potential surrogate markers of meningeal inflammation in MS, and imaging tools to apply to the clinical practice to early detect patients at high risk of elevated cortical damage and more severe progression and disability.
Dr. Magliozzi is author of 45 publications on peer-reviewed journal with a total of 3926 citations (by 2392 documents); h-index: 22.
Author Of 1 Presentation
HT05.01 - Presentation 01
Abstract
Abstract
Several experimental and clinical observations have suggested the presence of elevated inflammation, diffuse or organized in lymphoid structures that resemble secondary lymphoid organs, tertiary lymphoid structures (TLS), in the leptomeninges of either experimental animal model or post-mortem multiple sclerosis (MS) central nervous system (CNS), both in the brain and in the spinal cord. This feature, named lymphoid neogenesis, has been suggested to have a relevant role in maintaining intrathecal immune response in MS, as well as previosly shown in other chronic inflammatory diseases.
MS meningeal inflammation, particularly enriched in B cells and compartmentalized within cerebral sulci, is specifically linked to elevated demyelination and damage of the adjacent subpial cortical grey matter. In particular, elevated meningeal inflammationis associated with substantial “surface-in” gradient of cortical neuronal loss and microglia activation highest in the outer cortical layers, close to the cerebrospinal fluid (CSF)/pia boundary, compared to the inner ones.
The strict correlation between meningeal molecular profiling and paired CSF protein one in post-mortem MS cases with elevated cortical lesion load and aggressive disease course has suggested that meningeal infiltrates may represent one of the main intrathecal sources of inflammatory and cytotoxic factors that released in the CSF might orchestrate and/or exacerbate chronic local inflammation and following cortical pathology.
Similar intrathecal inflammatory pattern detected in naïve MS patients was able to predict 89% of the variance in cortical lesion volume and number at time of diagnosis and to distinguish patients at high risk of disease activity after 4 years follow-up.
Presenter Of 1 Presentation
HT05.01 - Presentation 01
Abstract
Abstract
Several experimental and clinical observations have suggested the presence of elevated inflammation, diffuse or organized in lymphoid structures that resemble secondary lymphoid organs, tertiary lymphoid structures (TLS), in the leptomeninges of either experimental animal model or post-mortem multiple sclerosis (MS) central nervous system (CNS), both in the brain and in the spinal cord. This feature, named lymphoid neogenesis, has been suggested to have a relevant role in maintaining intrathecal immune response in MS, as well as previosly shown in other chronic inflammatory diseases.
MS meningeal inflammation, particularly enriched in B cells and compartmentalized within cerebral sulci, is specifically linked to elevated demyelination and damage of the adjacent subpial cortical grey matter. In particular, elevated meningeal inflammationis associated with substantial “surface-in” gradient of cortical neuronal loss and microglia activation highest in the outer cortical layers, close to the cerebrospinal fluid (CSF)/pia boundary, compared to the inner ones.
The strict correlation between meningeal molecular profiling and paired CSF protein one in post-mortem MS cases with elevated cortical lesion load and aggressive disease course has suggested that meningeal infiltrates may represent one of the main intrathecal sources of inflammatory and cytotoxic factors that released in the CSF might orchestrate and/or exacerbate chronic local inflammation and following cortical pathology.
Similar intrathecal inflammatory pattern detected in naïve MS patients was able to predict 89% of the variance in cortical lesion volume and number at time of diagnosis and to distinguish patients at high risk of disease activity after 4 years follow-up.
Invited Speaker Of 1 Presentation
HT05.01 - Presentation 01
Abstract
Abstract
Several experimental and clinical observations have suggested the presence of elevated inflammation, diffuse or organized in lymphoid structures that resemble secondary lymphoid organs, tertiary lymphoid structures (TLS), in the leptomeninges of either experimental animal model or post-mortem multiple sclerosis (MS) central nervous system (CNS), both in the brain and in the spinal cord. This feature, named lymphoid neogenesis, has been suggested to have a relevant role in maintaining intrathecal immune response in MS, as well as previosly shown in other chronic inflammatory diseases.
MS meningeal inflammation, particularly enriched in B cells and compartmentalized within cerebral sulci, is specifically linked to elevated demyelination and damage of the adjacent subpial cortical grey matter. In particular, elevated meningeal inflammationis associated with substantial “surface-in” gradient of cortical neuronal loss and microglia activation highest in the outer cortical layers, close to the cerebrospinal fluid (CSF)/pia boundary, compared to the inner ones.
The strict correlation between meningeal molecular profiling and paired CSF protein one in post-mortem MS cases with elevated cortical lesion load and aggressive disease course has suggested that meningeal infiltrates may represent one of the main intrathecal sources of inflammatory and cytotoxic factors that released in the CSF might orchestrate and/or exacerbate chronic local inflammation and following cortical pathology.
Similar intrathecal inflammatory pattern detected in naïve MS patients was able to predict 89% of the variance in cortical lesion volume and number at time of diagnosis and to distinguish patients at high risk of disease activity after 4 years follow-up.