The associations between sugar-sweetened beverage (SSB) consumption and the risk of stroke, depression, cancer, and cause-specific mortality have not been determined, and the quantitative aspects of this link remain unclear. This meta-analysis therefore conducted a systematic review and dose-response analysis to determine their causal links. The database searches were conducted in PubMed, Cochrane library, Embase, Web of Science up to 10 November 2021. The intervention effects were evaluated by relative risk (RR) with 95% confidences (CI). Thirty-two articles met the inclusion criteria. Higher levels of SSB consumption significantly increased the risk of stroke (RR 1.12, 95% CI 1.03–1.23), depression (1.25, 1.11–1.41), cancer (1.10, 1.03–1.17), and all-cause mortality (1.08, 1.05–1.11) compared with none or lower SSB intake. The associations were dose-dependent, with per 250 mL increment of SSB intake daily increasing the risk of stroke, depression, cancer, and all-cause mortality by RR 1.09 (1.03–1.15), 1.08 (1.06–1.10), 1.17 (1.04–1.32), and 1.07 (1.03–1.11), respectively. The link was curved for depression and cancer risk (p_non-linear < 0.05). Subgroup analysis suggested that higher SSB intake increased ischemic stroke by 10%, CVD-caused mortality by 13%, and cancer-caused mortality by 6.0% than none or lower SSB consumption. It is suggested that SSB accounts for a leading risk factor of stroke, depression, cancer, and mortality, and that the risk rises in parallel with the increment of SSB intake (and is affected by participant characteristics).

Neuroinflammation is a major feature of type 2 diabetic mellitus (T2DM), adversely affecting hippocampal neurogenesis. However, the precise mechanism is not fully understood, and therapeutic approaches are currently lacking. Therefore, we determined the effects of exercise on neuroinflammation and hippocampal neurogenesis in T2DM mice, with a specific focus on understanding the role of the irisin and related cascade pathways in modulating the beneficial effects of exercise in these processes. Ten-week exercise significantly decreased T2DM-induced inflammation levels and markedly promoted hippocampal neurogenesis and memory function. However, these positive effects were reversed by 10 weeks of treatment with cyclo RGDyk, an inhibitor of irisin receptor signaling. Additionally, exercise helped reduce the M1 phenotype polarization of hippocampal microglia in diabetic mice; this effect could be reversed with cyclo RGDyk treatment. Moreover, exercise markedly increased the levels of fibronectin type III domain-containing protein 5 (FNDC5)/irisin protein while decreasing the expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and nuclear factor kappa-B (NF-κB) in the hippocampus of T2DM mice. However, blocking irisin receptor signaling counteracted the down-regulation of TLR4/MyD88/NF-κB in diabetic mice undergoing exercise intervention. Conclusively, exercise appears to be effective in reducing neuroinflammation and enhancing hippocampal neurogenesis and memory in diabetes mice. The positive effects are involved in the participation of the irisin/TLR4/MyD88/NF-κB signaling pathway, highlighting the potential of exercise in the management of diabetic-induced cognitive decline.

Purpose: To examine the effects of three types of school-based exercises on bone health and physical fitness function in Chinese boys and girls. Methods: One hundred and seventy-four Chinese boys and girls were randomly assigned into four groups: (1) sham exercise (ShEx); (2) high-impact exercise (HiEx); (3) high-impact exercise with various directions (HiExVi); and (4) high-intensity interval exercise (HiInEx). Speed of sound (SOS) and physical fitness parameters were determined before and after six-month intervention. Results: At the end of six-month intervention, participants in all groups show an increment of SOS compared with the baseline (p < 0.05), and the changes were higher in HiEx (mean: 38.878 m/s, 95% CI: 32.885~44.872, p = 0.001) and HiExVi groups (49.317 m/s, 42.737~55.897, p < 0.001) compared with ShEx group (20.049 m/s, 13.751~26.346). Six-month exercise training generated a reduction of percent of body fat (PBF) and waist–hip ratio (WHR) (p < 0.05). The decrease of PBF was greater in HiExVi (−1.222%, −1.820~−0.624, p = 0.012) and HiInEx groups (−1.395%, −1.809~−0.982, p = 0.003), whereas the reduction of WHR was larger in HiEx (−0.026, −0.039~−0.014, p = 0.009), HiExVi (−0.024, −0.036~−0.012, p = 0.021), and HiInEx groups (−0.035, −0.046~−0.024, p < 0.001) compared with ShEx group. Balance function (BLF), vital capacity (VC), standing long jump (SLJ), and sit up (SU) increased in all intervention groups (p < 0.05). The BLF increased in HiEx (6.332 s, 4.136~8.528, p = 0.001), HiExVi (10.489 s, 8.934~12.045, p < 0.001), and HiInEx groups (9.103 s, 7.430~10.776, p < 0.001) showed a greater change than that of ShEx group (1.727 s, 0.684~2.770). The increment of VC (273.049 mL, 199.510~346.587, p < 0.001) and SU (2.537 times/min, 0.639~4.435, p = 0.017) was higher in HiInEx group, whereas the accrual in SLJ was larger in HiExVi (7.488 cm, 4.936~10.040, p = 0.007) compared with ShEx group (58.902 mL, 7.990~109.814; −0.463 times/min, −2.003~1.077; 1.488 cm, −0.654~3.630). Conclusion: The brief school-based exercises were effective in improving schoolchildren’s health, but they showed different effects, with HiEx mostly improving bone health, HiInEx largely benefiting physical fitness function, and HiExVi enhancing both bone and physical fitness.

Although exercise is known to exert anti-inflammatory effects in neurodegenerative diseases, its specific impact and underlying mechanisms in Parkinson’s disease (PD) remain poorly understood. This study explores the effects of exercise on microglia-mediated neuroinflammation and apoptosis in a PD model, focusing on the role of irisin signaling in mediating these effects. Using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model, we found that a 10-week treadmill exercise regimen significantly enhanced motor function, reduced dopaminergic neuron loss, attenuated neuronal apoptosis, and alleviated neuroinflammation. Exercise also shifted microglia from a pro-inflammatory to an anti-inflammatory phenotype. Notably, levels of irisin, phosphorylated AMP-activated protein kinase (p-AMPK), and sirtuin 1 (Sirt1), which were decreased in the PD brain, were significantly increased following exercise. These beneficial effects were abolished by blocking the irisin receptor with cyclic arginine–glycine–aspartic acid–tyrosine–lysine (cycloRGDyk). Our results indicate that exercise promotes neuroprotection in PD by modulating microglial activation and the AMPK/Sirt1 pathway through irisin signaling, offering new insights into exercise-based therapeutic approaches for PD.

Recent advances in single-cell RNA sequencing (scRNA-seq) have substantially deepened our understanding of adult hippocampal neurogenesis (AHN), enabling the detection of neural stem cells, progenitors, and immature neurons in postmortem human brain tissue and revealing how these populations are altered in neurological disease. Additionally, scRNA-seq enables the identification of disease-specific cell subtypes and distinct gene expression signatures associated with neurological disorders, many of which are linked to alterations in AHN and cognitive function. Such cellular- and molecular-level insights into neurological disease mechanisms provide a strong foundation for the development of targeted therapeutic strategies. Indeed, scRNA-seq has also emerged as a powerful tool in drug discovery and development across multiple disease areas, including cancer, cardiovascular disorders, and neurological conditions. In this review, we offer a comprehensive and integrative perspective on the cellular and molecular landscape of human hippocampal neurogenesis, the pathological mechanisms underlying neurological disorders, and their implications for therapeutic development.