2009 | Josa M. Frischer, Stephan Bramow, Assunta Dal-Bianco, Claudia F. Lucchinetti, Helmut Rauscha, Manfred Schmidbauer, Henning Laursen, Per Soelberg Sorensen and Hans Lassmann
A study published in the journal BRAIN explores the relationship between inflammation and neurodegeneration in multiple sclerosis (MS) brains. The research analyzed 67 MS autopsy cases and 28 control cases, focusing on the interdependence of inflammation, neurodegeneration, and disease progression across different MS stages. The findings indicate that inflammation is present not only in acute and relapsing MS but also in secondary progressive (SPMS) and primary progressive (PPMS) MS. T- and B-cell infiltrates correlate with active demyelinating lesions, while plasma cell infiltrates are prominent in SPMS and PPMS, persisting even when T- and B-cell infiltrates decline. A strong association between inflammation and axonal injury was observed in both the global MS population and in progressive MS alone. In older patients with long disease duration, inflammatory infiltrates declined to levels similar to those in age-matched controls, and axonal injury was comparable. However, ongoing neurodegeneration in these patients, which exceeded that in normal controls, was attributed to confounding pathologies such as Alzheimer's or vascular disease. The study suggests a close association between inflammation and neurodegeneration in all MS lesions and disease stages, indicating that disease processes may cease in aged patients with long-standing disease. The results highlight the complex interplay between inflammation and neurodegeneration in MS, with implications for future therapeutic strategies.A study published in the journal BRAIN explores the relationship between inflammation and neurodegeneration in multiple sclerosis (MS) brains. The research analyzed 67 MS autopsy cases and 28 control cases, focusing on the interdependence of inflammation, neurodegeneration, and disease progression across different MS stages. The findings indicate that inflammation is present not only in acute and relapsing MS but also in secondary progressive (SPMS) and primary progressive (PPMS) MS. T- and B-cell infiltrates correlate with active demyelinating lesions, while plasma cell infiltrates are prominent in SPMS and PPMS, persisting even when T- and B-cell infiltrates decline. A strong association between inflammation and axonal injury was observed in both the global MS population and in progressive MS alone. In older patients with long disease duration, inflammatory infiltrates declined to levels similar to those in age-matched controls, and axonal injury was comparable. However, ongoing neurodegeneration in these patients, which exceeded that in normal controls, was attributed to confounding pathologies such as Alzheimer's or vascular disease. The study suggests a close association between inflammation and neurodegeneration in all MS lesions and disease stages, indicating that disease processes may cease in aged patients with long-standing disease. The results highlight the complex interplay between inflammation and neurodegeneration in MS, with implications for future therapeutic strategies.