Secondo alcuni ricercatori dell'Università di Bufallo (New York) l'attuale paradigma della sclerosi multipla, supportato solo parzialmente dalle lesioni istopatologiche della SM e dal suo modello animale (encefalite autoimmune sperimentale) considera la SM come una malattia prevalentemente autoimmune. Fino a poco tempo fa, la maggior parte dei fattori di rischio noti della SM sono stati interpretati nel contesto della teoria autoimmune, che non riesce ancora a spiegare perché le popolazioni geneticamente più vicine, esposte a simili fattori di rischio patogeni e/o ambientali, hanno una diversa incidenza della SM. Le terapie che ha parzialmente modulano il lato infiammatorio della patogenesi della SM, non riescono a raggiungere prestazioni simili in stadi della malattia più avanzati, quando sono presenti meno lesioni infiammatorie e maggiori neurodegenerazioni. Diversi studi hanno riportato un aumento della morbilità cardiovascolare nei pazienti con SM e che la comorbidità vascolari in qualsiasi momento durante il decorso della malattia aumenta il rischio di disabilità progressiva. Una condizione chiamata insufficienza venosa cronica cerebro spinale ha fornito una prospettiva diversa, la possibile associazione della sclerosi multipla con anomalie del sistema venoso. I loro recenti risultati hanno rivelato un aumento della prevalenza dell'insufficienza venosa cronica cerebro spinale associata alla progressione della malattia SM, così come con altri disturbi neurologici. D'altra parte, evidenze emerse recentemente indicano che esiste un'associazione tra le lipoproteine ed il metabolismo del colesterolo con la progressione della SM. Un peggioramento della scala di disabilità per pazienti affetti da SM è stato associato con un livello più alto di lipoproteine a bassa densità e di colesterolo totale, e livelli sierici più elevati di lipoproteine ad alta densità sono stati associati con un volume più basso delle lesioni pesate in T1. Si pensa che l'apolipoproteina A-1 e l'enzima antiossidante paraoxonasi siano associati a lipoproteine ad alta densità e contribuiscano alle sue proprietà antiossidanti ed anti-infiammatorie. E' stata anche recentemente dimostrata una significativa interdipendenza tra la vitamina D, uno dei più noti fattori di rischio ambientali per la SM, e la progressione della SM e il profilo sierico lipidico. Secondo gli autori è necessario un futuro lavoro in questa direzione per chiarire meglio il ruolo del metabolismo lipidico e della patologia vascolare nella patogenesi della SM.
Fonte italiana: http://www.facebook.com/notes/sandro-rasman/
The current paradigm of MS, supported only partially by MS lesion histopathology and its animal model (experimental allergic encephalomyelitis) considers MS to be a predominantly autoimmune disease. Until recently, most of the known risk factors for MS were interpreted in the context of the autoimmune theory, which still fails to explain why genetically close populations exposed to similar pathogens and/or environmental risk factors have different incidences of MS. Therapies which partially modulate the inflammatory arm of MS pathogenesis, fail to achieve similar benefits in later disease stages, when less inflammatory lesions and more neurodegeneration are present. Several studies have reported an increased cardiovascular morbidity in MS patients and that vascular comorbidity at any time during the disease course also increased the risk of progressive disability. A condition named chronic cerebrospinal venous insufficiency provided a different perspective, on the possible association of MS with the abnormalities of the venous system. Our recent findings revealed increased prevalence of chronic cerebrospinal venous insufficiency associated with MS disease progression as well as with other neurologic disorders. On the other hand, recently emerging evidence indicates that there is an association between lipoproteins and cholesterol metabolism and MS disease progression. Expanded disability status scale worsening was associated with higher baseline low-density lipoprotein and total cholesterol, and higher serum high-density lipoprotein levels were associated with lower contrast-enhancing T1-weigthed lesion volume. It is thought that apolipoprotein A-1 and paraoxonase anti-oxidant enzyme are associated with high-density lipoprotein and contribute to its anti-oxidant and anti-inflammatory properties. A significant inter-dependence was also recently demonstrated between vitamin D, one of the best known environmental risk factors for MS and MS disease progression and the serum lipid profile. Future work in this direction is required in order to better elucidate the role of lipid metabolism and vascular pathology in pathogenesis of MS.
Source: http://www.ingentaconnect.com/
Fonte italiana: http://www.facebook.com/notes/sandro-rasman/
The current paradigm of MS, supported only partially by MS lesion histopathology and its animal model (experimental allergic encephalomyelitis) considers MS to be a predominantly autoimmune disease. Until recently, most of the known risk factors for MS were interpreted in the context of the autoimmune theory, which still fails to explain why genetically close populations exposed to similar pathogens and/or environmental risk factors have different incidences of MS. Therapies which partially modulate the inflammatory arm of MS pathogenesis, fail to achieve similar benefits in later disease stages, when less inflammatory lesions and more neurodegeneration are present. Several studies have reported an increased cardiovascular morbidity in MS patients and that vascular comorbidity at any time during the disease course also increased the risk of progressive disability. A condition named chronic cerebrospinal venous insufficiency provided a different perspective, on the possible association of MS with the abnormalities of the venous system. Our recent findings revealed increased prevalence of chronic cerebrospinal venous insufficiency associated with MS disease progression as well as with other neurologic disorders. On the other hand, recently emerging evidence indicates that there is an association between lipoproteins and cholesterol metabolism and MS disease progression. Expanded disability status scale worsening was associated with higher baseline low-density lipoprotein and total cholesterol, and higher serum high-density lipoprotein levels were associated with lower contrast-enhancing T1-weigthed lesion volume. It is thought that apolipoprotein A-1 and paraoxonase anti-oxidant enzyme are associated with high-density lipoprotein and contribute to its anti-oxidant and anti-inflammatory properties. A significant inter-dependence was also recently demonstrated between vitamin D, one of the best known environmental risk factors for MS and MS disease progression and the serum lipid profile. Future work in this direction is required in order to better elucidate the role of lipid metabolism and vascular pathology in pathogenesis of MS.
Source: http://www.ingentaconnect.com/
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