A human translational model based on neuroplasticity for pharmacological agents potentially effective in Treatment-Resistant Depression: focus on dopaminergic system

作     者：Ginetta Collo Emilio Merlo Pich Ginetta Collo;Emilio Merlo Pich

作者机构：Department of Molecular and Translational MedicineSection of PharmacologyUniversity of BresciaBresciaItaly Department of BiomedicineUniversity of BaselBaselSwitzerland(Collo G)Neuroscience Therapeutic Area UnitTakeda Pharmaceuticals InternationalZurichSwitzerland Division of Brain ScienceImperial CollegeLondonUK(Merlo Pich E 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2020年第15卷第6期

页      面：1027-1029页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 10[医学] 

基　　金：funded by Ministry of Education University and Research(MIUR)ex-60%research fund University of Brescia Italy.Emilio Merlo Pich is employee of Takeda Pharmaceutical International AG 

主　　题：breakthrough plasticity translational 

摘      要：Major depressive disorder(MDD)is a common psychiatric condition characterized by two main symptoms,low mood and anhedonia.About 15–30%of people suffering from MDD do not respond to standard-of-care antidepressants,e.g.,the serotonin re-uptake inhibitors(SSRI),and are considered affected by Treatment-Resistant Depression(TRD).The neurobiology of this condition is presently unknown.Recent attempts of developing novel treatments for TRD have been driven by four major breakthroughs:(1)Increasing dopaminergic neurotransmission improves TRD symptoms;(2)Anhedonia occurs when central dopaminergic neurotransmission is low;(3)Enhanced neuroplasticity is critical for the action of antidepressants;(4)Ketamine shows antidepressant properties in TRD patients and triggers neuroplasticity in preclinical animal models.These breakthroughs are at the basis of a putative human translational cellular model for antidepressant agents that we are proposing in this article.The rationale is briefly described here.