Accumulating evidence has indicated that embryonic inflammation could accelerate age-associated cognitive impairment, which can be attributed to dysregulation of synaptic plasticity-associated proteins, such as RNA-binding proteins (RBPs). Staufen is a double-stranded RBP that plays a critical role in the modulation of synaptic plasticity and memory. However, relatively few studies have investigated how embryonic inflammation affects cognition and neurobiology during aging, or how the adolescent psychosocial environment affects inflammation-induced remote cognitive impairment. Consequently, the aim of this study was to investigate whether these adverse factors can induce changes in Staufen expression, and whether these changes are correlated with cognitive impairment. In our study, CD-1 mice were administered lipopolysaccharides (LPS, 50 μg/kg) or an equal amount of saline (control) intraperitoneally during days 15-17 of gestation. At 2 months of age, male offspring were randomly exposed to stress (S), an enriched environment (E), or not treated (CON) and then assigned to five groups LPS, LPS+S, LPS+E, CON, and CON+S. Mice were evaluated at 3-month-old (young) and 15-month-old (middle-aged). Cognitive function was assessed using the Morris water maze test, while Staufen expression was examined at both the protein and mRNA level using immunohistochemistry/western blotting and RNAscope technology, respectively. The results showed that the middle-aged mice had worse cognitive performance and higher Staufen expression than young mice. Embryonic inflammation induced cognitive impairment and increased Staufen expression in the middle-aged mice, whereas adolescent stress/an enriched environment would accelerated/mitigated these effects. Meanwhile, Staufen expression was closely correlated with cognitive performance. Our findings suggested embryonic inflammation can accelerate age-associated learning and memory impairments, and these effects may be related to the Staufen expression.The loss of cognitive function in Alzheimer's disease is pathologically linked with neurofibrillary tangles, amyloid deposition, and loss of neuronal communication. Cerebral insulin resistance and mitochondrial dysfunction have emerged as important contributors to pathogenesis supporting our hypothesis that cerebral fructose metabolism is a key initiating pathway for Alzheimer's disease. Fructose is unique among nutrients because it activates a survival pathway to protect animals from starvation by lowering energy in cells in association with adenosine monophosphate degradation to uric acid. The fall in energy from fructose metabolism stimulates foraging and food intake while reducing energy and oxygen needs by decreasing mitochondrial function, stimulating glycolysis, and inducing insulin resistance. When fructose metabolism is overactivated systemically, such as from excessive fructose intake, this can lead to obesity and diabetes. Herein, we present evidence that Alzheimer's disease may be driven by overactivation of cerebral fructose metabolism, in which the source of fructose is largely from endogenous production in the brain. Thus, the reduction in mitochondrial energy production is hampered by neuronal glycolysis that is inadequate, resulting in progressive loss of cerebral energy levels required for neurons to remain functional and viable. In essence, we propose that Alzheimer's disease is a modern disease driven by changes in dietary lifestyle in which fructose can disrupt cerebral metabolism and neuronal function. Inhibition of intracerebral fructose metabolism could provide a novel way to prevent and treat this disease.Background Braking force is a gait marker associated with gait stability. This study aimed to determine the alteration of braking force and its correlation with gait stability in Alzheimer disease (AD). Methods A total of 32 AD patients and 32 healthy controls (HCs) were enrolled in this study. Gait parameters (braking force, gait variability, and fall risk) in the walking tests of Free walk, Barrier, and Count backward were measured by JiBuEn® gait analysis system. https://www.selleckchem.com/products/kp-457.html Gait variability was calculated by the coefficient of variation (COV) of stride time, stance time, and swing time. Results The braking force of AD was significantly weaker than HCs in three walking tests (P less then 0.001, P less then 0.001, P = 0.007). Gait variability of AD showed significant elevation than HCs in the walking of Count backward (COVstride P = 0.013; COVswing P = 0.006). Fall risk of AD was significantly higher than HCs in three walking tests (P = 0.001, P = 0.001, P = 0.001). Braking force was negatively associated with fall risks in three walking tests (P less then 0.001, P less then 0.001, P less then 0.001). There were significant negative correlations between braking force and gait variability in the walking of Free walk (COVstride P = 0.018; COVswing P = 0.013) and Barrier (COVstride P = 0.002; COVswing P = 0.001), but not Count backward (COVstride P = 0.888; COVswing P = 0.555). Conclusion Braking force was weaker in AD compared to HCs, reflecting the worse gait stability of AD. Our study suggests that weakening of braking force may be a new gait marker to indicate cognitive and motor impairment and predict fall risk in AD.Background Recently, considerable research has been conducted to study the effects of transcranial direct current stimulation (tDCS) on balance control in older adults. We completed a comprehensive systematic review and meta-analysis to assess the efficacy of tDCS on balance control in this population. Methods A search strategy based on the PICOS principle was used to find the literatures in the databases of PubMed, EMBASE, EBSCO, Web of Science. The quality and risk of bias in the studies were independently assessed by two researchers. Results Ten studies were included in the systematic review. A meta-analysis was completed on six of these ten, with a total of 280 participants. As compared to sham (i.e., control), tDCS induced significant improvement with low heterogeneity in balance control in older adults. Specifically, tDCS induced large effects on the performance of the timed-up-and-go test, the Berg balance scale, and standing postural sway (e.g., sway area) and gait (e.g., walking speed) in dual task conditions (standardized mean differences (SMDs) = -0.