Abstract
Depression is a psychiatric disorder that has a significant health burden on patients and their families. Unfortunately, the current antidepressant medications that mainly target monoamine neurotransmitters have limited efficacy. Recent evidence has indicated that neuroinflammation participates in the genesis and development of depression, and interacts with other factors involved in depression. Therefore, exploring effective anti-inflammatory medications could be beneficial for the development of new treatment options for depression. Sirtuins are a unique class of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, which have seven members that can affect multiple downstream targets by deacetylation activity. Among these seven members, SIRT1 and SIRT2 have been shown to participate in the pathophysiology of inflammation in numerous studies. Thus, in this short article, we review the association of SIRT1 and SIRT2 activity and depression, and evidence of the effects of SIRT1 and SIRT2 modulators on inflammation in vitro and depressive-like behaviours in vivo.
Highlights
In this short article, we review the association of SIRT1 and SIRT2 activity and depression, and evidence of the effects of SIRT1 and SIRT2 modulators on inflammation in vitro and depressive-like behaviours in vivo
According to the data published by the World Health Organisation, over 264 million people of all ages suffer from depression, and approximately 800,000 people die from suicide every year [2]
The sirtuin family is a unique class of nicotinamide adenine dinucleotide (NAD+ )dependent deacetylases
Summary
Depression is one of the leading causes of disability [1]. According to the data published by the World Health Organisation, over 264 million people of all ages suffer from depression, and approximately 800,000 people die from suicide every year [2]. The main theories of the underlying pathophysiology of depression include deficiency of monoamine neurotransmitters such as serotonin, noradrenaline and dopamine in the central nervous system, dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, and reduction in brain-derived neurotrophic factor (BDNF). Excessive inflammatory cytokines can influence other mechanisms of depression by decreasing the production of serotonin and BDNF, fueling glutamate excitotoxicity and disrupting the HPA axis and hormone balance [8]. There are no medication options that target the inflammatory process applied in the clinical treatment of depression.
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