Cerebral blood flow self-regulation in depression

•Cerebral blood flow self-regulation (CBFSR) is impaired in depression.•Compromised CBFSR is affected by multiple mechanisms.•Many neurological symptoms in depressed patients are related to impaired CBFSR.•Impaired CBFSR has adverse effects on patients with depression. Depression is a common neurops...

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Veröffentlicht in:Journal of affective disorders 2022-04, Vol.302, p.324-331
Hauptverfasser: Liu, Min, He, Enling, Fu, Xiyao, Gong, Sizhu, Han, Yue, Deng, Fang
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Sprache:eng
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Zusammenfassung:•Cerebral blood flow self-regulation (CBFSR) is impaired in depression.•Compromised CBFSR is affected by multiple mechanisms.•Many neurological symptoms in depressed patients are related to impaired CBFSR.•Impaired CBFSR has adverse effects on patients with depression. Depression is a common neuropsychiatric disease with a high prevalence rate. Sleep problems, memory decline, dizziness and headaches are the most common neurological symptoms in depressed patients. Abnormality of cerebral blood flow (CBF) has been observed in depressive patients, but those patients did not have intracranial structural damage. Both of those phenomena might be related to cerebral blood flow self-regulation (CBFSR: cerebral blood flow self-regulation). CBFSR can maintain CBF relatively stable in response to changes in neurological and metabolic factors. Therefore, this review aimed to discuss CBFSR in depression. We searched for keywords such as "depression", "cerebral blood flow", "cerebral autoregulation", "cerebrovascular reactivity" and the words related to depression. We analyzed whether there is a change in the CBFSR in depression, further explored whether there is a relationship between the pathogenesis of depression and the CBFSR, and discussed the possible mechanism of impaired CBFSR in patients with depression. Discovered by the literature review, CBFSR is significantly impaired in depressed patients. The level of circulating markers of endothelial dysfunction, nitric oxide, inflammatory cytokines, glucocorticoid and monoamine neurotransmitters is mostly abnormal in depression, which affected the CBFSR to varying degrees. Limitations include the small number of direct studies about depression and CBFSR mechanisms. CBFSR is impaired in depression. The underlying mechanisms include endothelial dysfunction, overactivation of microglia and changes of cytokines, hyperactivation of the HPA axis, increased oxidative stress, monoamine neurotransmitter disorders, etc. These deepened our understanding of the clinical symptoms of depressed patients.
ISSN:0165-0327
1573-2517
DOI:10.1016/j.jad.2022.01.057