title: Glatiramer acetate could be a potential therapeutic agent for Parkinson's disease through its neuroprotective and anti-inflammatory effects.
abstract: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The hallmark pathologic feature of PD is dopamine deficiency, caused by the degeneration of nigrostriatal dopaminergic neurons. Current treatments for PD mainly address the dopaminergic features of the disease; however they do not modify the progression of neurodegeneration. The need for newer and more effective agents is consequently receiving a great deal of attention. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, can promote survival of injured dopaminergic nigrostriatal neurons in the rodent. Postmortem studies have suggested that BDNF deficiency may play a role in PD pathogenesis. This is further supported by the finding that BDNF administration has a therapeutic effect in animal models of PD. Glatiramer acetate (GA) is a collection of synthetic polypeptides approved for the treatment of relapsing-remitting multiple sclerosis. Preclinical studies have demonstrated that peripheral GA administration can enhance central BDNF activity and augment neurogenesis. Furthermore, PD has been associated with an inflammatory process in the brain. Animal studies have demonstrated that GA administration has a central anti-inflammatory effect through the release of anti-inflammatory cytokines. From the above evidence, GA could act as a potential therapeutic agent for PD by increasing central BDNF and by exerting an anti-inflammatory effect. With the recent finding that GA administration can prevent neuronal loss and cognitive decline in Alzheimer's disease double-transgenic mice, early GA treatment may also prevent neurodegeneration and manifestations of PD symptoms in subjects with familial Parkinson's disease.
authors.affiliation: Department of Psychiatry, Taipei Veterans General Hospital, No. 201 Shih-Pai Road, Sec. 2, 11217 Taipei, Taiwan sjtsai@vghtpe.gov.tw
authors.forename: Shih-Jen
authors.initials: SJ
authors.lastname: Tsai
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology / Q000628:therapy; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001921:Brain / Q000378:metabolism; D019208:Brain-Derived Neurotrophic Factor / Q000008:administration & dosage*; D016207:Cytokines / Q000378:metabolism; D004298:Dopamine / Q000172:deficiency / Q000378:metabolism; D000068717:Glatiramer Acetate; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D007249:Inflammation; D051379:Mice; D008822:Mice, Transgenic; D008962:Models, Theoretical; D009474:Neurons / Q000378:metabolism; D010300:Parkinson Disease / Q000188:drug therapy* / Q000473:pathology; D010455:Peptides / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D019208:Brain-Derived Neurotrophic Factor; D016207:Cytokines; D007166:Immunosuppressive Agents; D010455:Peptides; D000068717:Glatiramer Acetate; D004298:Dopamine