title: [Neuroprotection in the treatment of multiple sclerosis].
abstract: Atrophy, the wasting or shrinkage of tissue, of the nervous system is the main feature of neurodegeneration, i.e. the umbrella term for the progressive loss of structure or function of neurons. Loss of neurons due to cell death and axonal degeneration characterize neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease or amyotrophic lateral sclerosis. In these illnesses, it still has to be elucidated to which extent inflammation is part of the pathology. Conversely, in chronic inflammation of the central nervous system (CNS), atrophy has previously also been described and neurodegeneration is discussed as a pathologic feature. The most frequent chronic inflammatory disease of the CNS is multiple sclerosis (MS), which leads to devastating relapsing-remitting symptoms and disability during the relapses, increasingly during the course of disease in patients. Meanwhile it became clear that axons already reveal pathology early in the disease and neurons are affected in the cortex and the spinal cord, albeit to a different extent. The broadening of understanding neurodegenerative aspects of MS pathology demands and creates new therapeutic strategies. Current medication used in MS treatment as well as medications about to be approved are primarily anti-inflammatory therapies. By modulating the immune system and thereby blocking key steps of the pathology, the immunomodulation therapies in MS have a slight impact on disability progression. There is, however, clinical and experimental data concerning the potential neuroprotective properties of novel therapies. Combining anti-inflammatory and direct neuroprotective or even neuroregenerative therapy strategies would be a step forward in the treatment of multiple sclerosis.
authors.affiliation: Klinik und Poliklinik für Neurologie, Universitätsmedizin Mainz, Johannes-Gutenberg-Universität, Langenbeckstr. 1, 55131 Mainz, Deutschland. frauke.zipp@unimedizin-mainz.de
authors.forename: F
authors.initials: F
authors.lastname: Zipp
authors.forename: R
authors.initials: R
authors.lastname: Gold
mesh_terms: D000074323:Alemtuzumab; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000912:Antibodies, Neoplasm / Q000627:therapeutic use; D001369:Axons / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D001921:Brain / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D018450:Disease Progression; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D009416:Nerve Regeneration / Q000187:drug effects; D019636:Neurodegenerative Diseases / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D009474:Neurons / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D011379:Prognosis; D012183:Retrograde Degeneration / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D013116:Spinal Cord / Q000187:drug effects / Q000276:immunology / Q000473:pathology
chemical_list: D000893:Anti-Inflammatory Agents; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D007155:Immunologic Factors; D018696:Neuroprotective Agents; D000074323:Alemtuzumab