Center for Psychiatric Research, Psychiatric Hospital of Aarhus University Risskov, Denmark.
Front Psychiatry. 2013 Mar 4;4:8. doi: 10.3389/fpsyt.2013.00008. eCollection 2013.
Molecular mechanisms in the brain are assumed to cause the symptoms and severity of neuropsychiatric disorders. This review concerns the elusive nature of relationships between the severity of depressive disorders and neuromolecular processes studied by positron emission tomography (PET). Recent PET studies of human depression have focused on serotonergic, dopaminergic, muscarinic, nicotinic, and GABAergic receptors, as well as central processes dependent on monoamine oxidase, phosphodiesterase type 4, amyloid plaques, neurofibrillar tangles, and P-glycoprotein. We find that reliable causal links between neuromolecular mechanisms and relief from depressive disorders have yet to be convincingly demonstrated. This situation may contribute to the currently limited use of PET for exploring the neuropathways that are currently viewed as being responsible for beneficial effects of antidepressant treatment regimes.
大脑中的分子机制被认为是导致神经精神疾病症状和严重程度的原因。这篇综述涉及到通过正电子发射断层扫描(PET)研究的抑郁障碍严重程度与神经分子过程之间难以捉摸的关系。最近对人类抑郁症的 PET 研究集中在 5-羟色胺能、多巴胺能、毒蕈碱能、烟碱能和 GABA 能受体,以及依赖单胺氧化酶、磷酸二酯酶 4、淀粉样斑块、神经原纤维缠结和 P-糖蛋白的中枢过程。我们发现,神经分子机制与抑郁障碍缓解之间可靠的因果关系尚未得到令人信服的证明。这种情况可能导致目前 PET 在探索目前被认为对抗抑郁治疗方案有益影响负责的神经通路方面的有限应用。