Cigarette smoke-induced pulmonary impairment is associated with social recognition memory impairments and alterations in microglial profiles within the suprachiasmatic nucleus of the hypothalamus

Luca, Simone N. De; Chan, Stanley M H; Dobric, Aleksandar; Wang, Hao; Seow, Huei Jiunn; Brassington, Kurt; Mou, Kevin; Alateeq, Rana; Akhtar, Alina; Bozinovski, Steven; Vlahos, Ross

doi:10.1016/j.bbi.2023.02.005

Cited by 5 publications

(8 citation statements)

References 86 publications

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“…We have also shown that chronic cigarette smoke exposure induces a reactive astrocyte profile within the hippocampus (Dobric et al, 2022) and hypothalamus (De Luca et al, 2023). This reactive astrocyte profile was associated with endothelial cell tight junction protein impairment (reduction in ZO-1), thus reducing BBB integrity, compared to sham mice, leading to working memory impairments (Dobric et al, 2022).…”

Section: Senescence-associated Secretory Phenotypementioning

confidence: 73%

“…This is consistent with previous data showing that an acute treatment of mice, with the tobacco‐specific pro‐carcinogen compound, 4‐N‐methyl‐N‐nitrosamino‐1‐(3‐pyridyl)‐1‐butanone, for as little as 4 days, can induce robust changes in hippocampal microglial morphology (Ghosh et al, 2009 ). We have also shown that chronic cigarette smoke exposure induces a reactive astrocyte profile within the hippocampus (Dobric et al, 2022 ) and hypothalamus (De Luca et al, 2023 ). This reactive astrocyte profile was associated with endothelial cell tight junction protein impairment (reduction in ZO‐1), thus reducing BBB integrity, compared to sham mice, leading to working memory impairments (Dobric et al, 2022 ).…”

Section: Copd‐induced Ageing Within the Cnsmentioning

confidence: 86%

“…However, whether this is associated with accelerated cellular senescence and circadian rhythm disruption within the brain remains unknown. To the best of our knowledge, we were the first to demonstrate that, in mice, chronic exposure to cigarette smoke leads to a notable shift in circadian rhythm regulation profiles (reduced locomotor activity, respiratory exchange ratio [RER] and energy expenditure during the dark phase but increased VO 2 ), increased expression of the transcriptional repressor gene, Per2, and a reduced number of BMAL1-positive cells, compared with data from sham mice (De Luca et al, 2023). Within our preclinical cigarette smoke exposure model, we have previously shown a SASP milieu within the hippocampus and hypothalamus, with increases in pro-inflammatory cytokines and chemokines, oxidative stress markers as well as increased microglial and astrocyte activation (De Luca et al, 2022Dobric et al, 2022).…”

Section: Dysfunction Of the Circadian Rhythm Clock Promoted Progressionmentioning

confidence: 99%

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Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease‐induced neuropathological comorbidities

De Luca,

Vlahos

2023

British J Pharmacology

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Chronic Obstructive Pulmonary Disease (COPD) is a major incurable health burden, ranking as the 3rd leading cause of death worldwide, mainly driven by cigarette smoking. COPD is characterised by persistent airway inflammation, lung function decline, and premature aging with the presence of pulmonary senescent cells. This review proposes that cellular senescence, a state of stable cell cycle arrest linked to ageing; induced by inflammation and oxidative stress in COPD, extends beyond the lungs and impacts the systemic circulation. This pulmonary senescent profile will reach other organs via extracellular vesicles contributing to brain inflammation and damage, and increasing the risk of neurological comorbidities, such as stroke, cerebral small vessel disease, and Alzheimer's disease. The review explores the role of cellular senescence in COPD‐associated brain conditions and investigates the relationship between cellular senescence and circadian rhythm in COPD. Additionally, it discusses potential therapies, including senomorphic and senolytic treatments, as novel strategies to halt or improve COPD progression.

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Section: Senescence-associated Secretory Phenotypementioning

confidence: 73%

Section: Copd‐induced Ageing Within the Cnsmentioning

confidence: 86%

Section: Dysfunction Of the Circadian Rhythm Clock Promoted Progressionmentioning

confidence: 99%

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Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease‐induced neuropathological comorbidities

De Luca,

Vlahos

2023

British J Pharmacology

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“…Previous research has indicated that the buildup of amyloid-β (Aβ) in neuronal tissue in old mice may play a role in muscle atrophy and disruption of neuromuscular junctions(NMJ), which as the nexus between the nervous and muscular systems, is critical for input and dependable neural control of muscle force generation [11]. Additionally, pulmonary impairment has been linked to deficits in social recognition memory and changes in microglial profiles within the suprachiasmatic nucleus of the hypothalamus [12]. In instances of prolonged decline in pulmonary function, individuals may experience hypoxic conditions, which can have detrimental effects on neuronal oxygen homeostasis [13], may contributed to the onset and progression of cognitive impairment [14].…”

Section: Introductionmentioning

confidence: 99%

Cognition as mediator of pulmonary function and risk of sarcopenia among older adults

Hu,

Tang,

Zhan

2024

BMC Public Health

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Background The relationship between lung function and sarcopenia remains ambiguous. The primary aim of this study was to investigate the potential association between lung function and sarcopenia in the older adults, as well as to examine the mediating role of cognitive function in this relationship. Methods The participants were selected from a nationally representative population-based cohort in China. The peak expiratory flow (PEF) measurement was used to evaluate the lung function in older persons. The sarcopenia was diagnosed using the guidelines of the Asian Working Group for Sarcopenia (AWGS) in 2019. The Cox proportional hazard model was utilized to perform primary analyses of the relationship between PEF and sarcopenia. The mediating effect of cognitive function was evaluated using the counterfactual mediation method. Results This cohort study included 4,011 older adults (average age, 66.6 years; 53.3% males). During a follow-up period of 3.86 years, 349 individuals were diagnosed with sarcopenia. After adjusting for potential confounders, each one-standard-deviation increase in PEF was associated with a 28% reduction in the risk of sarcopenia (hazard ratio [HR]: 0.72; 95% confidence interval [CI]: 0.63, 0.80). There was a significant mediation of cognition for the association between PEF and incident sarcopenia, and the proportion mediated was 12.2% (95% CI: 4.5%, 23.1%). Conclusions Older adults with impaired lung function are more likely to develop sarcopenia. Nevertheless, cognition can explain only a small portion of this association. Thus, other potential pathways between lung function and sarcopenia must be elucidated.

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“…However, the mechanism underlying the relationship between ANU-ADRI and AD pathology remains unclear. Microglia-related neuroinflammation might explain how some risk factors in ANU-ADRI scores (e.g., depression and smoking) influence AD pathology [ 17 , 18 ]. Triggering receptor expressed on myeloid cell 2 (TREM2) is expressed mainly by microglia cell in the central nervous system (CNS) [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

ANU-ADRI scores, tau pathology, and cognition in non-demented adults: the CABLE study

Yin,

Gao,

et al. 2024

Alz Res Therapy

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Background It has been reported that the risk of Alzheimer’s disease (AD) could be predicted by the Australian National University Alzheimer Disease Risk Index (ANU-ADRI) scores. However, among non-demented Chinese adults, the correlations of ANU-ADRI scores with cerebrospinal fluid (CSF) core biomarkers and cognition remain unclear. Methods Individuals from the Chinese Alzheimer’s Biomarker and LifestyLE (CABLE) study were grouped into three groups (low/intermediate/high risk groups) based on their ANU-ADRI scores. The multiple linear regression models were conducted to investigate the correlations of ANU-ADRI scores with several biomarkers of AD pathology. Mediation model and structural equation model (SEM) were conducted to investigate the mediators of the correlation between ANU-ADRI scores and cognition. Results A total of 1078 non-demented elders were included in our study, with a mean age of 62.58 (standard deviation [SD] 10.06) years as well as a female proportion of 44.16% (n = 476). ANU-ADRI scores were found to be significantly related with MMSE (β = -0.264, P < 0.001) and MoCA (β = -0.393, P < 0.001), as well as CSF t-tau (β = 0.236, P < 0.001), p-tau (β = 0.183, P < 0.001), and t-tau/Aβ42 (β = 0.094, P = 0.005). Mediation analyses indicated that the relationships of ANU-ADRI scores with cognitive scores were mediated by CSF t-tau or p-tau (mediating proportions ranging from 4.45% to 10.50%). SEM did not reveal that ANU-ADRI scores affected cognition by tau-related pathology and level of CSF soluble triggering receptor expressed on myeloid cells 2 (sTREM2). Conclusion ANU-ADRI scores were associated with cognition and tau pathology. We also revealed a potential pathological mechanism underlying the impact of ANU-ADRI scores on cognition.

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Cigarette smoke-induced pulmonary impairment is associated with social recognition memory impairments and alterations in microglial profiles within the suprachiasmatic nucleus of the hypothalamus

Cited by 5 publications

References 86 publications

Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease‐induced neuropathological comorbidities

Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease‐induced neuropathological comorbidities

Cognition as mediator of pulmonary function and risk of sarcopenia among older adults

ANU-ADRI scores, tau pathology, and cognition in non-demented adults: the CABLE study

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