Association of depression with longitudinal changes in brain structure across the lifespan: A mendelian randomization study.

Understanding the impact of depression on brain aging benefits the prognosis of this disease and of the risk that other age-related brain disorders will develop in the same population. The aim of the present study was to explore the genetic effect of depression on longitudinal changes in brain structure throughout the lifespan using a Mendelian randomization approach. Summary data from a genome-wide association study of 195,321 to 377,277 participants in the FinnGen consortium were used to predict depression, anxiety disorders, mood disorders, and antidepressant use genetically.

High-fat diet induced hippocampal CREB dysfunction, cognitive impairment and depression-like behaviors via downregulation of interleukin-2 in the mice.

Background: Inhibition of hippocampal CREB signaling contributed to obesity-induced cognitive impairment. But, the potential mechanism by which obesity inhibits hippocampal CREB signaling is not clear. The aim of this study was to explore whether interleukin-2 played a intermediary role in this pathogenic effect in a high-fat diet model.

Phase-Amplitude Coupling Brain Networks in Children with Attention-Deficit/Hyperactivity Disorder.

In cognitive neuroscience, there is an increasing interest in identifying and understanding the synchronization of distinct neural oscillations with different frequencies that might support dynamic communication within the brain. This study explored the cross-frequency phase-amplitude coupling brain network characteristics of resting-state electroencephalograms between 30 children with attention-deficit/hyperactivity disorder (ADHD) and 30 age-matched typically developing children. Compared with control group, children with ADHD show increased coupling intensity and altered distribution patterns of dominant paired channels, especially in the δ-γ, θ-γ, α-γ, β-γ, and β-γ coupling networks.

MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells.

Neuroinflammation is a mechanism by which obesity or a high-fat diet leads to cognitive impairment. MiR-124, a highly expressed microRNA in the brain, can alleviate neuroinflammation by regulating microglial activation, but its mechanism is unclear. The aim of the study was to explore whether miR-124 exerted this effect through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells.

Exogenous IGF-1 improves tau pathology and neuronal pyroptosis in high-fat diet mice with cognitive dysfunction.

Insulin-like growth factor-1 (IGF-1) improves obesity-induced cognitive dysfunction, but its mechanism is not fully clarified. The aim of the study was to reveal whether IGF-1 treated cognitive dysfunction by improving tau pathology and neuronal pyroptosis in high-fat diet mice. During in vitro experiment, C57BL/6J mice were fed with high-fat diet, and were treated with PEG-IGF-1, IGF-1 receptor blocker AXL1717, HO-1 blocker Znpp IX or their combinations.

Inhibition of miR-129 Improves Neuronal Pyroptosis and Cognitive Impairment Through IGF-1/GSK3β Signaling Pathway: An In Vitro and In Vivo Study.

Pyroptosis is a programmed cell death process which is accompanied by inflammation. The aims of this in vitro and in vivo study were to reveal whether miR-129 contributed to neuronal pyroptosis and cognitive impairment and to further explore its mechanism involved. PC-12 cells were treated with LPS, miR-129 antagomir, AXL1717 (IGF-1 receptor blocker), or SB216763 (GSK3β blocker).

A Study on Resting EEG Effective Connectivity Difference before and after Neurofeedback for Children with ADHD.

Altered functional networks in attention deficit/hyperactivity disorder (ADHD) have been frequently reported, but effective connectivity has hardly been studied. Especially the differences of effective connectivity in children with ADHD after receiving neurofeedback (NF) training have been merely reported. Therefore, this study aimed to explore the effective networks of ADHD and the positive influence of NF on the effective networks.

IGF-1 Alleviates Mitochondrial Apoptosis through the GSK3β/NF-κB/NLRP3 Signaling Pathway in LPS-Treated PC-12 Cells.

Inflammation contributes to mitochondrial dysfunction and neuronal apoptosis. The aim of this study was to determine whether insulin-like growth factor-1 (IGF-1) alleviates mitochondrial apoptosis in lipopolysaccharide (LPS)-treated PC-12 cells, and to further explore the mechanism involved. Prepared PC-12 cells were treated with IGF-1, Mdivi-1 (DRP1 blocker), LY294002 (PI3K blocker), betulinic acid (NF-κB activator) or their combinations.

Exogenous IGF-1 alleviates depression-like behavior and hippocampal mitochondrial dysfunction in high-fat diet mice.

Background: Some evidence suggests that depression is more common in obese patients. This fact gives us a hint that obesity might be a promoter of depression, though a conclusion can not be drawn. The aim of the study was: (1) to confirm whether obesity induced by high-fat diet (HFD) promotes depression-like behaviors in mice, (2) to explore the protective role of insulin-like growth factor-1 (IGF-1) in such behavioral disorder of the animals and (3) to reveal whether mitochondrial mechanism was involved in such protective effect of the reagent.