中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (6): 1027-1029.doi: 10.4103/1673-5374.270305

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

人转化模型中促进神经可塑性:HNK在难治性抑郁症中的抗-隔膜效应的相关性

  

  • 出版日期:2020-06-15 发布日期:2020-07-01

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

Ginetta Collo1, Emilio Merlo Pich2   

  1. 1Department of Molecular and Translational Medicine, Section of Pharmacology, University of Brescia, Brescia, Italy; Department of Biomedicine, University of Basel, Basel, Switzerland  2Neuroscience Therapeutic Area Unit, Takeda Pharmaceuticals International, Zurich, Switzerland; Division of Brain Science, Imperial College, London, UK
  • Online:2020-06-15 Published:2020-07-01
  • Contact: Ginetta Collo, MD, collo@med.unibs.it;Emilio Merlo Pich, MD, emilio.merlo-pich@takeda.com.
  • Supported by:
    This work is 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.

摘要:

orcid: 0000-0003-1888-5049 (Ginetta Collo) 

         0000-0001-5478-235X (Emilio Merlo Pich)

Abstract: 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.