Bidirectional communication between brain and visceral white adipose tissue: Its potential impact on Alzheimer's disease

Huang, Xiao; Wang, Yanjiang; Xiang, Yang

doi:10.1016/j.ebiom.2022.104263

Cited by 6 publications

(7 citation statements)

References 209 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…studied on their associations with clinical characteristics and pathogenesis of AD. 6 In the present study, plasma levels of three CTRPs members were higher in the AD group than those in the CN group and were remarkably associated with the presence of AD, suggesting that CTRPs, as a newly discovered adipokine family, are also to be associated with AD.…”

Section: Discussionsupporting

confidence: 53%

“…Previously, we proposed a new concept of the brain–visceral adipose tissue axis and sorted out its potential involvement in the pathogenesis of AD, in which a key mediator is adipokines produced by the adipose tissue 6 . The adipose tissue is the main site producing and secreting CTRPs, and nominally traditional adipokines (e.g., leptin, resistin, adiponectin, chemerin, and lipocalin‐2) have been widely studied on their associations with clinical characteristics and pathogenesis of AD 6 . In the present study, plasma levels of three CTRPs members were higher in the AD group than those in the CN group and were remarkably associated with the presence of AD, suggesting that CTRPs, as a newly discovered adipokine family, are also to be associated with AD.…”

Section: Discussionmentioning

confidence: 99%

“…5 Previously, we proposed the concept of the brain-visceral adipose tissue axis and preliminarily analyzed its potential influence on the development of AD, in which adipokines secreted by adipose tissue may play multiple regulatory roles in Aβ metabolism, tau phosphorylation, hippocampal neurogenesis, synaptic plasticity, and neuroinflammation. 6 Of note, complement 1q (C1q)/ tumor necrosis factor (TNF)-related proteins (CTRPs) are a newly discovered adipokine family and are mainly secreted by the adipose tissue. 7 CTRPs have a common characteristic structure including four different domains, one of which is homologous to adiponectin.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Huang,

Zhao,

Wang

et al. 2024

CNS Neurosci Ther

Self Cite

View full text Add to dashboard Cite

AimsRecent evidence indicated the biological basis of complement 1q (C1q)/tumor necrosis factor (TNF)‐related protein (CTRP) 3, 4, and 14 for affecting brain structure and cognitive function. Thus, we aimed to investigate the association between plasma CTRPs with Alzheimer's disease (AD).MethodsA multicenter, cross‐sectional study recruited patients with AD (n = 137) and cognitively normal (CN) controls (n = 140). After the data collection of demographic characteristics, lifestyle risk factors, and medical history, plasma levels of tau phosphorylated at threonine 217 (pT217), pT181, neurofilament light (NfL), CTRP3, 4, and 14 were examined and compared. Multivariate logistic regression analysis was applied to determine associations of plasma CTPRs with the presence of AD. The correlation analysis was used to explore correlations between plasma CTPRs with scores of Mini‐Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Activities of Daily Living (ADL) scale, and Clinical Dementia Rating Sum of Boxes (CDR‐SB), and levels of plasma pT217, pT181, and NfL. Receiver‐operating characteristic (ROC) analysis and Delong's test were used to determine the diagnostic power of plasma CTPRs.ResultsPlasma levels of CTRP3, 4, and 14 were higher in AD group than those in CN group. After adjusting for conventional risk factors, CTRP3, CTRP4, and CTRP14 were associated with the presence of AD. In AD patients, CTRP3 was negatively correlated with scores of MMSE and MoCA, while positively correlated with ADL score, CDR‐SB score, pT217, and pT181; CTRP4 was positively correlated with CDR‐SB score, pT181, and NfL; CTRP14 was negatively correlated with MMSE score, while positively correlated with CDR‐SB score, pT217, and NfL. An independent addition of CTRP3 and 4 to the basic model combining age, sex, years of education, APOE4 status, BMI, TG, and HDL‐C led to a significant improvement in diagnostic power for AD, respectively.ConclusionsAll the findings preliminarily uncovered associations between plasma CTRPs and AD and suggested the potential of CTRPs as a blood‐derived biomarker for AD.

show abstract

Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Huang,

Zhao,

Wang

et al. 2024

CNS Neurosci Ther

Self Cite

View full text Add to dashboard Cite

show abstract

“…The occurrence and severity of WMLs are strongly associated with systemic inflammation 2 . Obesity is associated with systemic inflammation, which can lead to several diseases including type 2 diabetes mellitus, cardiovascular diseases, and neurodegenerative diseases 3,4 . Moreover, obesity in midlife increases the risk of dementia later in life 5,6 and is frequently associated with current WMLs 7 .…”

Section: Introductionmentioning

confidence: 99%

“…2 Obesity is associated with systemic inflammation, which can lead to several diseases including type 2 diabetes mellitus, cardiovascular diseases, and neurodegenerative diseases. 3,4 Moreover, obesity in midlife increases the risk of dementia later in life 5,6 and is frequently associated with current WMLs. 7 It has been suggested that systemic inflammation links obesity to WMLs.…”

Section: Introductionmentioning

confidence: 99%

Microbial lipopolysaccharide‐induced inflammation contributes to cognitive impairment and white matter lesion progression in diet‐induced obese mice with chronic cerebral hypoperfusion

et al. 2023

View full text Add to dashboard Cite

Aims White matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia‐induced cognitive impairment and WMLs by diet‐induced obesity, including lipopolysaccharide (LPS)‐triggered neuroinflammation via toll‐like receptor (TLR) 4. Methods Wild‐type (WT) and TLR4‐knockout (KO) C57BL/6 mice were fed a high‐fat diet (HFD) or low‐fat diet (LFD), and subjected to bilateral carotid artery stenosis (BCAS). Diet groups were compared for changes in gut microbiota, intestinal permeability, systemic inflammation, neuroinflammation, WML severity, and cognitive dysfunction. Results In WT mice, HFD induced obesity and increased cognitive impairment and WML severity compared with LFD‐fed mice following BCAS. HFD caused gut dysbiosis and increased intestinal permeability, and plasma LPS and pro‐inflammatory cytokine concentrations. Furthermore, HFD‐fed mice had higher LPS levels and higher neuroinflammatory status, including increased TLR4 expression, in WMLs. In TLR4‐KO mice, HFD also caused obesity and gut dysbiosis but did not increase cognitive impairment or WML severity after BCAS. No difference was found between HFD‐ and LFD‐fed KO mice for LPS levels or inflammatory status in either plasma or WMLs. Conclusion Inflammation triggered by LPS–TLR4 signaling may mediate obesity‐associated exacerbation of cognitive impairment and WMLs from brain ischemia.

show abstract

White adipose tissue distribution and amount are associated with increased white matter connectivity

Okudzhava,

Schulz,

Fischi‐Gomez

et al. 2024

Human Brain Mapping

View full text Add to dashboard Cite

Obesity represents a significant public health concern and is linked to various comorbidities and cognitive impairments. Previous research indicates that elevated body mass index (BMI) is associated with structural changes in white matter (WM). However, a deeper characterization of body composition is required, especially considering the links between abdominal obesity and metabolic dysfunction. This study aims to enhance our understanding of the relationship between obesity and WM connectivity by directly assessing the amount and distribution of fat tissue. Whole‐body magnetic resonance imaging (MRI) was employed to evaluate total adipose tissue (TAT), visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT), while MR liver spectroscopy measured liver fat content in 63 normal‐weight, overweight, and obese males. WM connectivity was quantified using microstructure‐informed tractography. Connectome‐based predictive modeling was used to predict body composition metrics based on WM connectomes. Our analysis revealed a positive dependency between BMI, TAT, SAT, and WM connectivity in brain regions involved in reward processing and appetite regulation, such as the insula, nucleus accumbens, and orbitofrontal cortex. Increased connectivity was also observed in cognitive control and inhibition networks, including the middle frontal gyrus and anterior cingulate cortex. No significant associations were found between WM connectivity and VAT or liver fat. Our findings suggest that altered neural communication between these brain regions may affect cognitive processes, emotional regulation, and reward perception in individuals with obesity, potentially contributing to weight gain. While our study did not identify a link between WM connectivity and VAT or liver fat, further investigation of the role of various fat depots and metabolic factors in brain networks is required to advance obesity prevention and treatment approaches.

show abstract

Bidirectional communication between brain and visceral white adipose tissue: Its potential impact on Alzheimer's disease

Cited by 6 publications

References 209 publications

Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Microbial lipopolysaccharide‐induced inflammation contributes to cognitive impairment and white matter lesion progression in diet‐induced obese mice with chronic cerebral hypoperfusion

White adipose tissue distribution and amount are associated with increased white matter connectivity

Contact Info

Product

Resources

About