Connecting Parkinson's Disease and Drug Addiction: Common Players Reveal Unexpected Disease Connections and Novel Therapeutic Approaches

被引:31
作者
Gramage, Esther [1 ]
Herradon, Gonzalo [1 ]
机构
[1] Univ CEU San Pablo, Lab Pharmacol & Toxicol, Madrid 28668, Spain
关键词
Pleiotrophin; midkine; drug abuse; neurodegeneration; GDNF; beta-catenin; PROTEIN-TYROSINE PHOSPHATASES; RECEPTOR-TYPE-Z; ANAPLASTIC LYMPHOMA KINASE; PLEIOTROPHIN GENE-EXPRESSION; BETA/ZETA SIGNALING PATHWAY; COCAINE-SEEKING BEHAVIOR; LONG-TERM POTENTIATION; STRUCTURE-BASED DESIGN; NECROSIS-FACTOR-ALPHA; NEUROTROPHIC FACTOR;
D O I
10.2174/138161211795164103
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Parkinson's disease (PD) is generally a sporadic disease, and only a small proportion of cases have a clear genetic component. During the last few years, a possible specific cause triggering death of dopaminergic neurons in the substantia nigra, drug of abuse-induced neurotoxicity, is being considered as a potential mechanism to develop PD, especially in the case of abuse of amphetamine and its derivatives. Recent evidences have shown pleiotrophin, a growth factor with important functions in remodeling and repair of injured neural tissue, as an important factor involved in the pathogenesis of both diseases by preventing neurodegeneration in Parkinson's disease, neurotoxicity induced by drug abuse and by its ability to modulate drugs addictive effects. This review discusses targeting growth factors such as glial-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) to treat Parkinson's disease and/or drug addiction and compiles recent evidences to propose the pleiotrophin/receptor protein tyrosine phosphatase beta/zeta signaling pathway as a new therapeutic target to treat Parkinson's disease and to prevent drug of abuse-induced neurotoxicity and addictive effects.
引用
收藏
页码:449 / 461
页数:13
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