Carrera-González Maria Del Pilar, Cantón-Habas Vanesa, Rich-Ruiz Manuel
Department of Nursing, Pharmacology and Physiotherapy, Faculty of Medicine and Nursing, University of Córdoba, Maimonides Institute of Biomedical Research of Córdoba (IMIBIC), Reina Sofia University Hospital, Spain.
Experimental and Clinical Physiopathology Research Group CTS-1039, Department of Health Sciences, Faculty of Health Sciences, University of Jaén, Spain.
Adv Clin Exp Med. 2022 May;31(5):469-473. doi: 10.17219/acem/149897.
Population aging that we are currently witnessing has led to an increase in chronic age-related diseases, with dementia and depression being highlighted. Several studies establish a relationship between dementia and depression, although without defining the mechanism that links them. Some studies establish depression as a prodrome of dementia, while others consider it a risk factor for dementia. One of the events that is common between dementia and depression is the inflammatory process. In depression, an increase in inflammatory cytokines has been described, which would justify the serotonergic, noradrenergic and dopaminergic dysfunction of depression. This increase entails altering the activity of the hypothalamic-pituitary-adrenal (HPA) axis, thus linking chronic stress to depression, and the consequent weakening of the blood-brain barrier (BBB), facilitating the passage of pro-inflammatory factors. In this line, recent studies suggest that inflammation could direct the development of the pathogenesis of dementia, particularly Alzheimer's disease (AD), once the pathology has begun. In addition, sustained exposure to pro-inflammatory cytokines characteristic of aging could alter the microglial function and the expression of enzymes responsible for amyloid peptide metabolism, aggravating the pathological process. In view of the involvement of the inflammatory process in both conditions, it is necessary to investigate the events which both conditions share, such as the inflammatory process, to know the involvement of the inflammatory process in both dementia and depression, possible relationship of these 2 conditions, and consequently, to establish the clinical approach to both conditions.
我们目前正在经历的人口老龄化导致了与年龄相关的慢性疾病增多,其中痴呆症和抑郁症尤为突出。多项研究证实了痴呆症与抑郁症之间存在关联,尽管尚未明确两者之间的联系机制。一些研究认为抑郁症是痴呆症的前驱症状,而另一些研究则将其视为痴呆症的危险因素。痴呆症和抑郁症的一个共同特征是炎症过程。在抑郁症中,炎症细胞因子增加,这可以解释抑郁症中血清素能、去甲肾上腺素能和多巴胺能功能障碍的原因。这种增加会改变下丘脑-垂体-肾上腺(HPA)轴的活性,从而将慢性应激与抑郁症联系起来,并导致血脑屏障(BBB)减弱,促进促炎因子的通过。在这方面,最近的研究表明,一旦病理过程开始,炎症可能会主导痴呆症,尤其是阿尔茨海默病(AD)发病机制的发展。此外,持续暴露于衰老特有的促炎细胞因子可能会改变小胶质细胞功能以及负责淀粉样肽代谢的酶的表达,从而加重病理过程。鉴于炎症过程在这两种疾病中的作用,有必要研究两者共有的事件,如炎症过程,以了解炎症过程在痴呆症和抑郁症中的作用、这两种疾病可能的关系,从而确定针对这两种疾病的临床治疗方法。