Neurodegeneration in autoimmune demyelination: recent mechanistic insights reveal novel therapeutic targets.
Multiple sclerosis (MS) is the most common chronic demyelinating disease of the central nervous system (CNS) and the major cause of neurological disability in young adults in Western countries. In spite of intensive research efforts, treatment options established to date do not sufficiently prevent the accumulation of tissue damage and clinical disability in patients with MS. We here describe recently identified molecules responsible for the inflammatory and the neurodegenerative processes in MS and its animal model, experimental autoimmune encephalomyelitis (EAE), and review new treatment options targeting both aspects of this disease.
Aktas
Orhan
O
Institute for Neuroimmunology, Neuroscience Research Center, Charité -- Universitätsmedizin Berlin, Germany.
Waiczies
Sonia
S
Zipp
Frauke
F
D000214:Acyl Coenzyme A / Q000378:metabolism; D000818:Animals; D002392:Catechin / Q000031:analogs & derivatives / Q000627:therapeutic use; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental; D006801:Humans; D009103:Multiple Sclerosis / Q000150:complications* / Q000235:genetics / Q000473:pathology; D009410:Nerve Degeneration / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000502:physiology; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism
D000214:Acyl Coenzyme A; D018696:Neuroprotective Agents; D053221:TNF-Related Apoptosis-Inducing Ligand; C008047:3-hydroxy-3-methylglutaryl-coenzyme A; D002392:Catechin; C045651:epigallocatechin gallate