Higher inflammation and cerebral white matter injury associated with cognitive deficit in asthmatic patients with depression

Abstract

Background Depression is a common co-morbidity in asthma, worsening asthma control and impairing patient's quality of life. Previous studies have reported a higher risk of cognitive de cit in depression. However, few research has focused on the cognitive status of asthmatic patients with depression. Evidence showed that in ammation may play an important role in both asthma and depression. Moreover, cerebral white matter injury, which could be induced by in ammation, has been associated with depression. The present study aimed to assess the cognitive function and explore the potential mechanism in patients with asthma, depression and comorbidity. Methods We admitted four groups: Asthma comorbid Depression group (A + D, n = 26), Depression group (D, n = 25), Asthma group (A, n = 33) and Normal controls (N, n = 28). Cognitive function was assessed by Montreal Cognitive Assessment (MoCA). Various in ammatory cytokines were measured, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), high-mobility group box 1(HMGB1) and Netrin-1. Cerebral white matter injury was assessed by serum myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG), and their correlations with cognitive performance were calculated. Results A + D group showed the highest incidence of cognitive de cit with speci c affected cognitive domain. Compared to N group, serum levels of IL-6, HMGB1, Netrin-1, MBP and MOG were signi cantly elevated in A + D group. MOG level was negatively correlated with MoCA score. Conclusion Patients with comorbid condition presented more de nite, severe cognitive de cit and higher level of in ammatory cytokines. Cerebral white matter injury may account for the cognitive de cit in these patients and MOG could be a potential biomarker of this process.

Acupuncture Exerts Antidepressant Effects in Rats of Chronic Unpredictable Mild Stress: The Involvement of Inflammation in Amygdala and Brain-Spleen Axis

“…Besides, HMGB1 could promote the action of other DAMPs as an internal cellular stress, thus further increasing in ammation and neuroin ammation (25). Previous studies reported that the expression of HMGB1 and TLR4 were both upregulated in the brains of patients with depression (21) and in stress-induced rats(68). In this study, the expression of HMGB1 and TLR4 were elevated under CUMS in rats' amygdalae and spleens with downregulating effects of acupuncture.…”

“…High-mobility group box 1 (HMGB1) is critical in inducing and promoting the occurrence of in ammation and neuroin ammation (19,20). Studies indicate that HMGB1 can be up-regulated when stressed, accompanied with the increasing expression of its receptor in toll-like receptor 4 (TLR4) (21,22). TLR4 is an immune regulator of neuroimmune and neuroendocrine interactions in stress and depression (23).…”

Serum levels of high mobility group box‐1 protein (HMGB1) and soluble receptors of advanced glycation end‐products (RAGE) in depressed patients treated with electroconvulsive therapy

“…Previous studies have reported that blood levels of HMGB1 are higher in depressed patients with asthma, 19 and that patients with high blood levels of HMGB1 during acute cerebral infarction are more likely to experience a depressive state 3 months later 20 . In addition, the HMGB1‐RAGE pathway is known to be involved in various inflammatory diseases (diabetes, rheumatoid arthritis, inflammatory kidney disease, heart disease, tumor growth, chronic obstructive pulmonary disease) 21–25 .…”

Порушення Когнітивних Функцій При Хронічних Захворюваннях Органів Дихання

“…Досліджено чіткий зв'язок між ураженням білої речовини головного мозку за даними МРТ та когнітивними порушеннями у хворих на бронхіальну астму [26]. Дослідження свідчать про позитивний кореляційний зв'язок між пошкодженням білої речовини, визначеним за допомогою сироваткового мієлінового основного білка і мієлінового олігодендроцитарного глікопротеїну та рівнем цитокінів (ІЛ-1, ФНП-α, HMGB1-білок, Нетрин-1) у пацієнтів з бронхіальною астмою, що свідчить про вплив системного запалення на структурні зміни мозку в таких хворих [27].…”