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Schematic of the role of metabolic glutamate receptor 1 in brain synaptic plasticity. Our previous studies showed that aluminium increased the expression of metabolic glutamate receptor 1 (mGluR1) and decreased the learning and memory function of animals. Group I mGluRs regulate N-methyl-D-aspartic acid receptor (NMDAR) function through the phospholipase C (PLC)/phosphatidylinositol diphosphate (PIP2)/diacylglycerol (DAG)/protein kinase C (PKC) signalling pathway. PKC is the key factor in cross-talk between mGluR1 and NMDARs. Group I mGluRs coupled with the Gq protein activate PLC, and promote hydrolysis of PIP2 to inositol triphosphate (IP3) and DAG. DAG promotes the translocation and activation of PKC, while IP3 promotes the release of Ca2+ stored in the endoplasmic reticulum and further activates PKC through cascade reactions. PKC phosphorylates the C-terminal sites of the NR1, NR2A, and NR2B subunits of NMDAR, relieving blockage of the NMDAR channel by Mg2+ and increasing the influx of Ca2+. The increased intracellular Ca2+ concentration leads to changes of synaptic plasticity after a series of cascade reactions. LTP, long-term potentiation. • Al exposure inhibits synaptic plasticity in rats. • Al induced synaptic plasticity inhibition is associated with mGluR1, PKC, and NMDARs. • mGluR1 regulates PKC and NMDAR in synaptic plasticity inhibition induced by Al. The main symptoms of Alzheimer's disease (AD) is the loss of learning and memory ability, of which biological basis is synaptic plasticity. Aluminium has been found to cause changes in synaptic plasticity, but its molecular mechanism was unclear. In this study, Sprague-Dawley rats were injected with aluminium maltol (Al(mal) 3) through the lateral ventricle to establish an AD-like model. Y-maze, electrophysiological measurements, Golgi staining, scanning electron microscopy, quantitative real-time polymerase chain reaction, and western blot techniques were used to investigate regulation of the metabolic glutamate receptor 1 (mGluR1) in synaptic plasticity impairment induced by Al(mal) 3. The results showed that Al(mal) 3 inhibited the induction and maintenance of long-term potentiation in the hippocampal CA1 region. During this process, the expression of mGluR1 was up-regulated and it inhibited the expression and phosphorylation of the N-methyl-D-aspartic acid receptors (NMDARs). This mainly affected NMDAR1 and NMDAR2B but did not affect protein kinase C expression. [ABSTRACT FROM AUTHOR]

To evaluate the risk of cognitive impairment in workers with plasma aluminum concentrations and lifestyles using a Bayesian network (BN). In 2019, 476 male workers in the Shanxi Aluminum factory were investigated. We measured plasma aluminum concentrations in workers by inductive coupled plasma mass spectrometry (ICP MS) and tested workers' cognitive function by the MoCA scale. We collected the data of lifestyle by the occupational Workers' Health questionnaire and express the influence of lifestyle on cognition by the OR value (95 %CI) of logistic regression. A Bayesian network model was used to predict the risk of cognitive dysfunction. The subjects were divided into a cognitively normal group and cognitively impaired group according to MoCA scores. There were statistically significant differences in age, education level, alcohol consumption, physical exercise, reading, aluminum length of service and blood aluminum concentration between the two groups (P < 0.05). The plasma aluminum concentration in the cognitive impairment group was 1.68 times higher than that in the cognitive normal group. Four groups were established according to the quartile of blood aluminum concentration of the subjects, namely, Group Q1 (<14.95 μg/L), Q2 group (14.95–32.96 μg/L), Q3 group (32.96–56.62 μg/L), and Q4 group (>56.62 μg/L). Binary logistic regression analysis showed that in the adjustment variable Model2, drinking, short sleep, long sleep, and mobile phone use increased the risk of cognitive impairment by 1.505(0.99,2.289), 1.269(0.702,2.295), 1.125(0.711,1.781) and 1.19(0.779,1.82), respectively, compared with their reference values. The risk of cognitive impairment from reading and exercise was 0.7(0.398,1.232) and 0.787(0.51,1.217), respectively, compared with those of no reading and no exercise. The risk of cognitive impairment of blood aluminum concentration in the Q2, Q3, and Q4 groups was 2.103(1.092,4.051), 1.866(0.955,3.644) and 3.679(1.928,7.020), respectively, compared with that in the Q1 group. Compared with age <40 , the risk of cognitive impairment of age ≥40 was 2.515(1.508,4.193) (P < 0.05). Bayesian network model results showed that if all participants had plasma aluminum concentrations higher than Q4, the prevalence of cognitive impairment was 54.5 %. The prevalence of cognitive impairment was 75.0 % if all participants had plasma aluminum levels above Q4, were older than 40, smoked, drank alcohol, used a cell phone for more than 2 h, slept for more than 8 h, did not exercise, and did not read. Our findings suggest that both poor lifestyle and occupational aluminum exposure may affect cognitive function. Workers must maintain a reasonable lifestyle and reduce aluminum exposure, which can control the occurrence of cognitive impairment. • To investigate the effect of aluminum exposure on cognitive dysfunction in workers. • To predict and analyze the risk of cognitive dysfunction caused by lifestyle. • Healthy lifestyle is recommended for occupational aluminum workers. [ABSTRACT FROM AUTHOR]

Individuals with abnormal fasting plasma glucose (FPG) may be more susceptible to lung diseases associated with environmental pollutants. A cross-sectional survey of 629 workers in 2017 and a panel study of 304 workers from 2014 to 2019 were performed in China. The results showed that elevated total hydroxylated polycyclic aromatic hydrocarbon (ΣOH-PAH) concentration was associated with lower the percentage of predicted forced vital capacity (FVC%) among high-FPG workers (β for the cross-sectional analysis: −1.78%, 95%CI: −2.92%, −0.64%; β for the panel study: −1.10%, 95%CI: −2.19%, −0.02%). The absolute value of the cross-lagged path coefficient from FPG to FVC% (β 2 = −0.096) was significantly greater than that from FVC% to FPG (β 1 = 0.037). Our results suggest that FPG abnormalities may precede the lung function decline induced by PAH exposure and that high-FPG and high ΣOH-PAH levels have an interactive effect on lung function decline. [Display omitted] • The association between PAH and lung function was influenced by FPG. • Causal relationship in temporal order was analyzed by cross-lagged panel analyses. • Fasting glucose abnormalities precede FVC% decline. • FPG and PAH had interaction effects on the decline in lung function. [ABSTRACT FROM AUTHOR]