LEADER 02211 am 22006733u 450 001 9910156503903321 005 20221206093324.0 010 $a90-04-28695-0 024 7 $a10.1163/9789004286955 035 $a(CKB)2670000000575428 035 $a(SSID)ssj0001489306 035 $a(PQKBManifestationID)11920261 035 $a(PQKBTitleCode)TC0001489306 035 $a(PQKBWorkID)11453759 035 $a(PQKB)10659579 035 $a(OCoLC)894352626 035 $a(nllekb)BRILL9789004286955 035 $a(WaSeSS)IndRDA00120787 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/33503 035 $a(PPN)184918537 035 $a(EXLCZ)992670000000575428 100 $a20200608d1973 uy 0 101 0 $aeng 135 $aurmn#---uuuua 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 14$aThe demographic evolution of Surinam 1920-1970 $ea socio-demographic analysis /$fH. E. 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Great progress has been made in identifying the molecular mechanisms that can be utilized to develop highly efficacious treatments for MS patients. Since the middle of the last century, when studies using an inflammatory autoimmune model of MS i.e. experimental autoimmune encephalitis (EAE) were initiated, research on MS has since led to an enormous growth of knowledge. The limitations arising from these animal models have been partially compensated by insights generated from histopathological, immunological, genetic, imaging and clinical studies of MS. The importance of T cells and, recently of B cells, in MS has been elucidated and the significance of CNS resident cells, particularly in the progressive course of MS has been highlighted. The importance of environmental factors and genetic predisposition have also been recognized and the interaction between th e individual and its environment seems to play key roles in the pathogenesis of this disease. However, definite causative agent(s) or single gene(s) involved in MS still remain unidentified. A deeper understanding of the immunological pathways involved goes hand in hand with further improving therapy for MS. Focal inflammation in MS, caused by de novo CNS infiltration, can be prevented effectively using peripherally-acting drugs. However, diffuse CNS intrinsic inflammation and neurodegeneration are not targeted by the current arsenal of therapeutics and patients with progressive disease courses remain difficult to treat. Generating insights into pathophysiological processes and the clinical translation of this knowledge have been a formula of success for treating inflammatory diseases. The future will show whether this will hold true for CNS-trapped inflammation and neurodegeneration and whether the ultimate goal - truly curing MS - will be possible. 517 $aMultiple Sclerosis – From Bench to Bedside 517 $aMultiple Sclerosis ? 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