Adiponectin Levels Are Associated with White Matter Lesions (WMLs) and Cognitive Impairment

Quan, Hui; Yu, Tongya; Lin, Yingying; Pan, Jie; Mao, Bingjie; Wang, Xuan; Xie, Junchao; Liu, Xueyuan; Zhao, Yanxin

doi:10.1155/2022/9943250

Cited by 2 publications

(1 citation statement)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It protects the brain from cerebral ischemic injury, neurodegenerative diseases such as Alzheimer’s disease, as well as psychological disorders including post-traumatic stress disorder, anxiety, and depression ( Hu et al, 2015 ; Na et al, 2017 ; Zhang et al, 2017 ; Bloemer et al, 2018 ; Wu, 2019 ; Polito et al, 2020 ; Li et al, 2021 ). Adiponectin deficiency is associated with increased white matter lesions, increased mortality post-ischemic stroke, and decreased cognitive function in adults ( Efstathiou et al, 2005 ; Quan et al, 2022 ). A study in newborn rats shows that exogenous adiponectin can attenuate hypoxia-ischemia-induced brain injury by binding to its receptors and upregulating AMPK signaling ( Xu et al, 2018 ).…”

Section: Therapeutic Agents That Can Regulate Pgc-1α Activitymentioning

confidence: 99%

PGC-1α activity and mitochondrial dysfunction in preterm infants

2022

View full text Add to dashboard Cite

Extremely low gestational age neonates (ELGANs) are born in a relatively hyperoxic environment with weak antioxidant defenses, placing them at high risk for mitochondrial dysfunction affecting multiple organ systems including the nervous, respiratory, ocular, and gastrointestinal systems. The brain and lungs are highly affected by mitochondrial dysfunction and dysregulation in the neonate, causing white matter injury (WMI) and bronchopulmonary dysplasia (BPD), respectively. Adequate mitochondrial function is important in providing sufficient energy for organ development as it relates to alveolarization and axonal myelination and decreasing oxidative stress via reactive oxygen species (ROS) and reactive nitrogen species (RNS) detoxification. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) is a master regulator of mitochondrial biogenesis and function. Since mitochondrial dysfunction is at the root of WMI and BPD pathobiology, exploring therapies that can regulate PGC-1α activity may be beneficial. This review article describes several promising therapeutic agents that can mitigate mitochondrial dysfunction through direct and indirect activation and upregulation of the PGC-1α pathway. Metformin, resveratrol, omega 3 fatty acids, montelukast, L-citrulline, and adiponectin are promising candidates that require further pre-clinical and clinical studies to understand their efficacy in decreasing the burden of disease from WMI and BPD in preterm infants.

show abstract

Section: Therapeutic Agents That Can Regulate Pgc-1α Activitymentioning

confidence: 99%

PGC-1α activity and mitochondrial dysfunction in preterm infants

2022

View full text Add to dashboard Cite

show abstract

Circulating adipokines and MRI markers of brain aging in middle-aged adults from the community

Satizabal,

Himali,

Conner

et al. 2024

Journal of Alzheimer’s Disease

View full text Add to dashboard Cite

Background Midlife obesity is related to late-onset dementia. Studying adipose tissue-secreted adipokines in the context of brain aging may help us understand this association. Objective To investigate associations between adipokines and brain MRI markers in middle-aged adults from the Third-Generation cohort of the Framingham Heart Study. Methods Serum adiponectin, retinol-binding protein 4 (RBP4), fetuin-A, and Fatty Acid-Binding Protein 4 (FABP4) concentrations were measured by enzymatic immunoassays. MRI measures included total brain, cortical gray matter, hippocampal (total and anterior), lateral ventricular, and white matter hyperintensity volumes. We used linear regression models to separately relate adipokine concentrations to MRI measures, adjusting for potential confounders. Results We included 1882 participants (mean age of 48 ± 8 years, 54% women). Higher RBP4 concentrations were related to markers of brain atrophy, including smaller total (Beta ± standard error, −0.05 ± 0.02; p = 0.014) and cortical gray brain volumes (−0.06 ± 0.02; p = 0.004), and larger lateral ventricular volumes (0.06 ± 0.02; p = 0.006). Additionally, higher RBP4 (−0.06 ± 0.03; p = 0.042), Fetuin-A (−0.06 ± 0.03; p = 0.039), and FABP4 (−0.09 ± 0.03; p = 0.008) concentrations were associated with smaller anterior hippocampal volumes. Most associations remained after additional adjustment for vascular risk factors. In exploratory analyses, higher FABP4 was related to larger total brain in non-obese participants, and to smaller anterior hippocampal volumes in obese participants. Finally, higher adiponectin concentrations were related to smaller cortical gray, only in non-obese participants. Conclusions Our results suggest that adipokines are associated with markers of brain atrophy during midlife. Further studies are needed to replicate these findings and elucidate any potential mechanisms contributing to abnormal brain aging.

show abstract

Adiponectin Levels Are Associated with White Matter Lesions (WMLs) and Cognitive Impairment

Cited by 2 publications

References 26 publications

PGC-1α activity and mitochondrial dysfunction in preterm infants

PGC-1α activity and mitochondrial dysfunction in preterm infants

Circulating adipokines and MRI markers of brain aging in middle-aged adults from the community

Contact Info

Product

Resources

About