This study aimed to analyze the association between Attention Deficit/Hyperactivity Disorder (ADHD) and Internet addiction (IA). A systematic literature search was performed in four online databases in total including CENTRAL, EMBASE, PubMed and PsychINFO. Observational studies (case-control, cross-sectional and cohort studies) measuring the correlation between IA and ADHD were screened for eligibility. Two independent reviewers screened each article according to the predetermined inclusion criteria. A total of 15 studies (2 cohort studies and 13 cross-sectional studies) met our inclusion criteria and were included in the quantitative synthesis. Meta-analysis was conducted using RevMan 5.3 software. A moderate association between IA and ADHD was found. Individuals with IA were associated with more severe symptoms of ADHD, including the combined total symptom score, inattention score and hyperactivity/impulsivity score. Males were associated with IA, whereas there was no significant correlation between age and IA. IA was positively associated with ADHD among adolescents and young adults. Clinicians and parents should pay more attention to the symptoms of ADHD in individuals with IA, and the monitoring of Internet use of patients suffering from ADHD is also necessary. Longitudinal studies controlling for baseline mental health are needed.

How glia affect neurite outgrowth during neural development has not been well elucidated. In the present study, we found that disruption of lactate production using 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) and isofagomine significantly interfered with neurite outgrowth and that exogenous application of L-lactate rescued neurite growth failure. Monocarboxylate transporter-2-knockout, which blocked the lactate shuttle in neurons, showed a remarkable decrease in the length of axons and dendrites. We further demonstrated that Akt activity was decreased while glycogen synthase kinase 3β (GSK3β) activity was increased after astrocytic glycogen phosphorylase blockade. Additionally, GSK3βSer9 mutation reversed neurite growth failure caused by DAB and isofagomine. Our results suggested that lactate transportation played a critical role in neural development and disruption of the lactate shuttle in quiescent condition also affected neurite outgrowth in the central nervous system.

Fatty amide hydrolase (FAAH) is a key degradation enzyme of the endocannabinoid system, mainly responsible for the hydrolysis of arachidonic acid ethanolamine (AEA). Previous investigations have shown that FAAH is involved in a series of biological processes, such as inflammation, immune regulation, and transmembrane signal transduction of neurons. Endogenous cannabinoids and cannabinoid receptors have been reported to participate in the regulation of bone homeostasis by regulating the differentiation of osteoblasts and osteoclasts. We hypothesized that FAAH may play an important role in osteoclastogenesis based on the above evidence. The present study found that the FAAH expression was increased at both mRNA and protein levels during RANKL‐induced osteoclastogenesis. Pharmacological and genetic inhibition of FAAH in bone marrow‐derived macrophages (BMMs) inhibited osteoclastogenesis, F‐actin ring formation, bone resorption, and osteoclast‐specific gene expression in vitro. Moreover, intragastric administration of the FAAH inhibitor PF‐04457845(PF) ameliorated ovariectomy (OVX)‐induced bone loss in mice. Further investigation revealed that nuclear factor κB (NF‐κB) and mitogen‐activated protein kinase (MAPK) pathways were inhibited by PF treatment and FAAH knockdown. RNAseq indicated that the IL17 pathway was blocked by PF, and administration of recombinant murine IL17 protein could partially restore osteoclastogenesis and activate NF‐κB and MAPK pathways. To sum up, our findings demonstrate that targeting FAAH could be a promising candidate strategy for treating osteoclast‐related diseases, especially osteoporosis.