Circadian syndrome (CircS) was recently proposed and referred to several common chronic diseases that showed a tight association with circadian disruption. This study included 15,594 participants from the National Health and Nutrition Examination Survey during 2003–2020. Survey-weight regression was used to examine the relationship between coffee consumption and CircS in the US population. Potential confounders were adjusted in the analysis. Mediation analysis was conducted to explore the mediating role of serum alkaline phosphatase (ALP) in the above relationship. After multivariate adjustment, participants with coffee consumption between one and two cups/day had significant reductions in CircS (OR: 0.976 with 95

Xylene is a widely encountered volatile organic compound, while little is known about its relationship with type 2 diabetes mellitus (T2DM) as well as possible roles of miR-181b-5p and miR-106b-5p, which are multifunctional microRNAs observed to be implicated in glucose metabolism, and the possible mechanisms. These uncharted territories warrant further investigation. In this case-control study of 138 newly developed T2DM adult patients and 138 matched healthy controls, urinary xylene exposure biomarkers (2-methyl hippuric acid [2MHA]; 3-methyl hippuric acid [3MHA]; 2MHA+3MHA [ΣUXYM]) and plasma miR-181b-5p/miR-106b-5p were measured. Relationships among xylene exposure biomarkers, miR-181b-5p/miR-106b-5p, and T2DM were estimated by generalized linear or logistic models. Potential roles of miR-181b-5p/miR-106b-5p in xylene-T2DM relationship were explored by mediation analyses. Network toxicology and molecular docking were performed to explore the hypothesis-generating pathway linking xylene and T2DM. We observed 2MHA (odds ratio=3.12; 95% confidence interval [CI]: 1.86∼5.24), 3MHA (2.12; 1.45∼3.10), ΣUXYM (2.33; 1.54∼3.54), miR-181b-5p (1.51; 1.25∼1.83), and miR-106b-5p (1.72; 1.42∼2.10) were positively related to T2DM odds. 2MHA was positively related to miR-181b-5p (β=0.40; 95% CI: 0.02∼0.78) and miR-106b-5p (0.56; 0.14∼0.98), which further accounted for 10.25% and 17.75% of the 2MHA-T2DM association, respectively. Peroxisome proliferator-activated receptor (PPAR) signaling pathway was enriched in the xylene-T2DM link, with potential molecular targets (estrogen receptor 1 [ESR1], etc.) identified. Target relationships between miR-181b-5p/miR-106b-5p and PPAR/ESR1 were predicted. Conclusively, exposure of general adults to xylene was positively associated with T2DM, which was partially explained by miR-181b-5p and miR-106b-5p, and PPAR signaling pathway and targets like ESR1 might be involved in the possible mechanisms.

Alzheimer's disease (AD) is a complex disease with unknown etiology and pathogenesis. We described a combined analysis of murine proteomics and microbiomics to find potential therapeutic targets of different doses of xanthohumol (Xn), with the goal of providing a biological basis for the treatment of early AD. Xn improved the spatial learning and memory ability of APP/PS1 mice; this was associated with an increased number of newborn neurons in the subgranular zone (SGZ) and dentate gyrus (DG) and a decreased inflammatory response. 108 proteins were significantly changed after 0.5 mg/kg Xn treatment while only 72 proteins changed by 5 mg/kg Xn. Eight significant microbiota were modulated by different doses of Xn at line discriminant analysis (LDA) score 3.0, but only three of which were regulated by 0.5 mg/kg Xn at LDA score 4.0. In addition, Xn treatment could significantly regulate the pathways of neurodegeneration- multiple diseases in the hippocampus and the penicillin and cephalosporin biosynthesis and atrazine degradation pathways in the gut. Interestingly, Nefl protein validated by correlation analysis was found in the common signaling pathway. 0.5 mg/kg Xn was able to reverse the correlation between hippocampal proteins and gut microbiota. Xn treatment significantly improved cognitive function in AD transgenic mice. Different doses of Xn caused significant differences in protein expression and flora composition and abundance, suggesting that the doses of Xn should be selected with caution, and low dose may be better in the prevention of AD.

Objective This study investigated the association between lactate-to-albumin ratio at admission to the pediatric intensive care unit and in-hospital all-cause mortality. Methods A retrospective cohort study was conducted using data from a large pediatric electronic database that included 9,689 critically ill children. The primary exposure variable was the first lactate-to-albumin ratio, which was analyzed as a continuous variable, while the outcome variable was in-hospital mortality. Multiple regression was employed to assess the relationship between lactate-to-albumin ratio and mortality, adjusting for potential confounders, such as length of hospital stay, sex, and other laboratory indicators. Results The results of the study revealed a significant positive correlation between the lactate-to-albumin ratio and in-hospital all-cause mortality. After adjustment, the regression coefficient (β) was4.05 (95% CI: 3.40 to 4.70, P < 0.01), indicating that a higher lactate-to-albumin ratio was associated with a high mortality risk. Tertile analysis showed that a high lactate-to-albumin ratio had significantly higher mortality rates than the low group, and sex-stratified analyses revealed a consistent positive correlation among both males and females.Additionally, and the association was most pronounced in all intensive care unit (ICU) patients. Conclusion This study highlights the potential of the lactate-to-albumin ratio as a predictive marker for critically ill pediatric patients in intensive care units. These findings underscore the importance of monitoring this ratio to evaluate patient risk and emphasize the need for further extensive multicenter studies to validate these findings.

Background: Neuronal excitotoxicity and metabolic decline, which begin in the early stages of Alzheimer’s disease (AD), pose challenges for effective amelioration. Our previous work suggested that the natural compound xanthohumol, the most abundant prenylated flavonoid in hops, prevents memory deficits in APP/PS1 mice; however, the underlying mechanisms remain unclear. Methods: This study utilized APP/PS1 mice and cutting-edge omics techniques to investigate the effects of xanthohumol on hippocampal proteome, serum metabolome, and microbiome. Results: Our findings revealed that xanthohumol reduces the postsynaptic overexpression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, N-methyl-D-aspartate, and metabotropic glutamate receptors, but enhances ATP synthesis and mitophagy in the young AD hippocampus. Further mechanistic analyses suggested systemic regulatory effects, particularly on the decreasing glutamate synthesis in the blood and intestines of AD mice following xanthohumol administration. Conclusions: These results underscore the potential of xanthohumol in mitigating AD pathology through multifaceted mechanisms, sparking interest and curiosity in its preventive and therapeutic potential in AD.

Alzheimer’s disease (AD) has an increasing prevalence, complicated pathogenesis and no effective cure. Emerging evidences show that flavonoid compounds such as xanthohumol (Xn) could play an important role as a dietary supplement or traditional Chinese herbal medicine in the management of diseases such as AD. This study aims to analyze the target molecules of Xn in the prevention and treatment of AD, and its potential mechanism from the perspective of metabolites. APP/PS1 mice 2- and 6-months old were treated with Xn for 3 months, respectively, the younger animals to test for AD-like brain disease prevention and the older animals to address therapeutic effects on the disease. Memantine (Mem) was selected as positive control. Behavioral tests were performed to assess the course of cognitive function. Urine samples were collected and analyzed by high-performance liquid chromatography (HPLC) with tandem mass spectrometry (MS/MS) coupled with online Compound Discoverer software. Morris Water Maze (MWM) tests showed that Xn, like Mem, had a therapeutic but not a preventive effect on cognitive impairment. The expression levels of urinary metabolites appeared to show an opposite trend at different stages of Xn treatment, downregulated in the prevention phase while upregulated in the therapy phase. In addition, the metabolic mechanisms of Xn during preventive treatment were also different from that during therapeutic treatment. The signaling pathways metabolites nordiazepam and genistein were specifically regulated by Xn but not by Mem in the disease prevention stage. The signaling pathway metabolite ascorbic acid was specifically regulated by Xn in the therapeutic stage. In conclusion, dietary treatment with Xn altered the urinary metabolite profile at different stages of administration in APP/PS1 mice. The identified potential endogenous metabolic biomarkers and signal pathways open new avenues to investigate the pathogenesis and treatment of AD.

The article takes the distribution and development history of the Qinzhou Riding House Cluster as an entry point, discusses the architectural characteristics and historical and cultural significance of the Qinzhou Riding House Cluster, and combines the relevant theories of community development and protection of historic districts with the actual problems faced by the Qinzhou Riding House in the development and protection of the Cluster, analyzes the main causes of the problems, and discusses the development and preservation strategies for the riding house area of Qinzhou in general, respectively, and provides strategic opinions on the preservation of historic and cultural districts and the development of urban public space respectively, in terms of the general ideas and overall strategies. It also discusses the development and preservation strategy of Qinzhou Riding Building area in general, respectively from the general idea and the overall strategy, and provides strategic opinions on the preservation of historical and cultural neighborhoods and the development of urban public space in Qinzhou area respectively.

Parabens and triclosan (TCS) have been extensively applied in personal care products (PCPs) as preservatives and antibacterial agents. However, their potentiality to disrupt the neurological system has induced increasing concern. The elderly population is at a higher risk of neurodegenerative disorder, although research on its association with PCP exposure remains scarce. Here, we measured the urinary levels of four parabens, TCS, and an oxidative stress marker among 540 participants from the Shenzhen aging-related disorder cohort during 2017-2018. The Mini-Mental State Examination (MMSE) was used to assess the cognitive status of participants. Their demographic, dietary, and behavioral factors were collected via questionnaire survey. Among the four paraben analogs, the median concentration of methyl parabens (MeP) was the highest (Low-risk group: 1.21 ng/ mL, High-risk group: 1.64 ng/mL). TCS and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were detected in more than 90% of the samples. Weighted quantile sum regression and quantile-based g-computation showed that the combined effect of all analytes was positively associated with the level of 8-OHdG. BtP, EtP and MeP were identified as the major contributors to the joint effect. After stratification by gender, females exhibited more pronounced changes in urinary 8-OHdG level than males. However, the positive correlation between co-exposure to parabens and TCS and cognitive impairment was not significant (p > 0.05) in both models, which warrants investigation with the larger sample size.

ObjectiveIndependent and interactive effects of multiple metals levels in urine on the risk of hyperuricemia (HUA) in the elderly were investigated.MethodsA total of 6,508 individuals from the baseline population of the Shenzhen aging-related disorder cohort were included in this study. We detected urinary concentrations of 24 metals using inductively coupled plasma mass spectrometry, fitted unconditional logistic regression models, and the least absolute shrinkage and selection operator regression models for the selection of metals as well as unconditional stepwise logistic regression models and restricted cubic spline logistic regression models for assessing the associations of urinary metals and HUA risk, and finally applied generalized linear models to determine the interaction with urinary metals on the risk of HUA.ResultsUnconditional stepwise logistic regression models showed the association between urinary vanadium, iron, nickel, zinc, or arsenic and HUA risk (all P < 0.05). We revealed a negative linear dose–response relationship between urinary iron levels and HUA risk (Poverall < 0.001, Pnonliner = 0.682), a positive linear dose–response relationship between urinary zinc levels and HUA risk (Poverall < 0.001, Pnonliner = 0.513), and an additive interaction relationship between urinary low-iron and high-zinc levels and HUA risk (RERI = 0.31, 95% CI: 0.03–0.59; AP = 0.18, 95%CI: 0.02–0.34; S = 1.76, 95%CI: 1.69–3.49).ConclusionUrinary vanadium, iron, nickel, zinc, or arsenic levels were associated with HUA risk, and the additive interaction of low-iron (<78.56 μg/L) and high-zinc (≥385.39 μg/L) levels may lead to a higher risk of HUA.

Epidemiological studies using conventional statistical methods have reported an association between individual metal exposure and hyperuricemia (HUA). There is also evidence that diet may influence HUA development, although the available data are inconsistent. We therefore used an elastic net regression (ENR) model to screen the usefulness of various environmental and dietary factors as predictors of HUA in a large sample cohort. This study included 6217 subjects drawn from the Shenzhen Aging Related Disorder Cohort. We obtained information on the subjects' dietary habits via face-to-face interviews and used inductively coupled plasma mass spectrometry (ICP-MS) to measure the urinary concentrations of 24 metals to which elderly persons in large urban areas may be exposed. An elastic net regression (ENR) model was generated to screen the utility of the metals and dietary factors as predictors of HUA, and we demonstrated the superiority of the ENR model by comparing it to a traditional logistic regression model. The identified predictors were used to create a clinically usable nomogram for identifying patients at risk of developing HUA. The area under curve (AUC) value of the final model was 0.692 for the training set and 0.706 for the test set. Important predictors of HUA were Zn, As, V, and Fe as well as consumption of wheat, beans, and rice; the corresponding estimated odds ratios and 95% confidence intervals were 1.091 (0.932,1.251), 1.190 (1.093,1.286), 0.924 (0.793,1.055), 0.704 (0.626,0.781), 0.998 (0.996,1.001), 0.993 (0.989,0.998), and 1.001 (0.998,1.002), respectively. In contrast to previous studies, we found that both urinary metal concentrations and dietary habits are important for predicting HUA risk. Exposure to specific metals and consumption of specific foods were identified as important predictors of HUA, indicating that the incidence of this disease could be reduced by reducing exposure to these metals and promoting improved dietary habits.

N -nitrosodimethylamine (NDMA) is an environmental and food contaminant, but limited data to concern whether NDMA has adverse effects on the brain. This study first determined the concentration of NDMA in foods from aquaculture markets in Shenzhen, then analyzed the effects on C57BL/6 mice and further evaluated on the urine samples of elderly Chinese residents with normal cognition (NC, n = 144), cognitive decline (CD, n = 116) and mild cognitive impairment (MCI, n = 123). The excessive rate of NDMA in foods was 3.32% (27/813), with a exceeding range of 4.78–131.00 μg/kg. Behavioral tests showed that 60 days treatment of mice with 3 mg/kg NDMA reduced cognitive performance. Cognitive impairment in human was significantly associated with sex, educational levels, length of residence in Shenzhen, household registration, passive smoking, rice, fresh vegetables, bacon products. NDMA was detected in 55.4% (212/383) of urine samples, with a median concentration of 0.23 μg/L (1.20 × 10 –7 –157.39 μg/L). The median concentration for NC, CD and MCI were 0.32, 0.27, and 0 μg/L, respectively. The urinary NDMA concentration had a strong negative correlation with cognitive impairment ( Kendall’s Tau-b = −0.89, P = 0.024). The median estimated daily intake (EDI) of NDMA was determined to be 6.63 ng/kg-bw/day. Taken together, there appears to be an association between NDMA and human and murine cognition, which provides a new clue to Alzheimer’s disease (AD).

Diabetic neuropathy is the most prevalent complication of diabetes mellitus. Although the precise etiology of this neurological disorder has yet to be defined, elevated blood glucose promotes anerobic glycolysis; this produces excess advanced glycation end‐products, many of which have a pyrrole structure. Here, we test the hypothesis that protein pyrrole adducts are associated with elevated glucose indices and some clinical features of diabetic diffuse neuropathies.

Abstract Introduction Diabetic neuropathy is the most prevalent complication of diabetes mellitus. Although the precise etiology of this neurological disorder has yet to be defined, elevated blood glucose promotes anerobic glycolysis; this produces excess advanced glycation end‐products, many of which have a pyrrole structure. Here, we test the hypothesis that protein pyrrole adducts are associated with elevated glucose indices and some clinical features of diabetic diffuse neuropathies. Method We investigated the levels of plasma pyrrole adducts and adjusted urinary pyrrole adducts in a group of elderly persons (n = 516, age 60–79) residing in the District of Luohu, Shenzhen, China between 2017 and 2018. Symptoms of distal symmetric polyneuropathy (DSPN) and resting heart rate, a measure of autonomic nervous system function, were collected from participants (n = 258) with elevated glucose indices. Result Protein pyrrole adducts showed a strong correlation with glucose indices before and after adjustment for age and estimated glomerular filtration rates. Stratified analysis showed that the medians and interquartile values of pyrrole adducts grew as glucose indices of the subgroups increased. Participants with symptoms of DSPN and sinus tachycardia presented elevated levels of plasma pyrrole adducts. Conclusion This study provides a novel link between glucose indices and the etiology of diabetic diffuse neuropathies.

Discovering new and effective drugs for the treatment of Alzheimer’s disease (AD) is a major clinical challenge. This study focuses on chemical modulation of the gut microbiome in an established murine AD model. We used the 16S rDNA sequencing technique to investigate the effect of xanthohumol (Xn) on the diversity of intestinal microflora in 2-month- and 6-month-old APP/PS1 mice, respectively. APP/PS1 and wild-type mice were treated by gavage with corn oil with or without Xn every other day for 90 days. Prior to and following treatment, animals were tested for spatial learning, cognitive and memory function. We found Xn reduced cognitive dysfunction in APP/PS1 mice and significantly regulated the composition and abundance of gut microbiota both in prevention experiments (with younger mice) and therapeutic experiments (with older mice). Differential microflora Gammaproteobacteria were significantly enriched in APP/PS1 mice treated with Xn. Nodosilineaceae and Rikenellaceae may be the specific microflora modulated by Xn. The penicillin and cephalosporin biosynthesis pathway and the atrazine degradation pathway may be the principal modulation pathways. Taken together, oral treatment with Xn may have a neuroprotective role by regulating the composition of intestinal microflora, a result that contributes to the scientific basis for a novel prophylactic and therapeutic approach to AD.

BackgroundAccumulating evidence suggests that alterations in liver function may play an important role in the pathogenesis of Alzheimer’s disease (AD). However, it remains unclear whether there is any relationship between lower liver function and cognitive impairment among the elderly.MethodsFrom 2017 to 2018, we recruited 7,201 older people (over 60 years old) from 51 community health centers in the Luohu District of Shenzhen City. According to the Mini-Mental State Examination (MMSE) score and education level, participants were divided into a cognitive impairment group (n = 372) and a normal cognitive function group (n = 6,829). Nonparametric test, chi-square tests, and binary logistic regression were used to analyze the data.ResultsCognitive impairment group exhibits older age, more female sex, lower education level, and lower levels of albumin and triglyceride. Additionally, the aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio was mainly distributed in the range of 1.17 to 1.3 in the cognitive impairment group, and 0.85 to 1.00 in the normal cognitive function group (χ2 = 10.02, p = 0.04). Binary logistic regression showed that cognitive impairment was significantly associated with age (OR = 0.934, 95%CI: 0.886–0.985, p = 0.017), female sex (OR = 2.255, 95%CI: 1.761–2.888, p < 0.001), lower education level (less than senior high school) (OR = 11.509, 95%CI: 9.064–14.613, p < 0.001), and lower albumin (OR = 1.023, 95%CI: 1.004–1.043, p = 0.011).ConclusionExcept for age, female sex, and lower education level, lower level of albumin and elevated AST to ALT ratio correlate with cognitive impairment. Whether lower liver function plays a role in AD needs to be further studied.

The wide application of organophosphorus flame retardants (OPFRs) in consumer products leads to their ubiquitous occurrence. The neurotoxicity of OPFRs has been raised, whereas evidence from the elderly population were rather scarce. Hence, a case-control study was conducted based on the Shenzhen Aging-related Disorder Cohort. A total of 184 cases [Mini-mental State Examination (MMSE) < 24] and 795 participants as controls (MMSE ≥24) were recruited. Eight metabolites of OPFRs (m-OPFRs) in urine samples were measured, including bis(2-butoxyethyl) phosphate (BBOEP), bis(2-chloroethyl) phosphate (BCEP), bis(1-chloro-2-propyl) phosphate (BCIPP), bis(1,3-dichloro-2-propyl) phosphate (BDCIPP), dibutyl phosphate (DBP), di-o-cresyl phosphate (DOCP), di-p-cresyl phosphate (DPCP) and diphenyl phosphate (DPHP). The detection frequencies of m-OPFRs ranged from 88.8 % to 95.4 %. BCEP had the highest median concentration (0.93 μg/L), followed by BCIPP (0.32 μg/L), DPHP (0.27 μg/L) and DBP (0.20 μg/L). Significant correlations were found between all pairs of urinary m-OPFRs with correlation coefficients ranging from 0.22 to 0.71 (p < 0.05). Logistic regression models showed that urinary concentrations of BDCIPP (adjusted odds ratio [OR]: 1.25, 95 % confidential interval [CI]: 1.04–1.50) and DBP (adjusted OR: 1.10, 95 % CI: 1.01–1.20) were positively associated with lower cognitive functions. Furthermore, a nonlinear dose-response relationship was found between urinary BDCIPP concentration and cognitive decline. To our knowledge, this is the first report on OPFR exposure and cognitive impairment among elderly population. Further toxicological tests of BDCIPP and DBP are needed to illustrate these results.

The expression of a gene requires not only a normal coding sequence but also intact regulatory regions, which can be located at large distances from the target genes, as demonstrated for an increasing number of developmental genes. In previous mutation studies of the role of FOXL2 in blepharophimosis syndrome (BPES), we identified intragenic mutations in 70% of our patients. Three translocation breakpoints upstream of FOXL2 in patients with BPES suggested a position effect. Here, we identified novel microdeletions outside of FOXL2 in cases of sporadic and familial BPES. Specifically, four rearrangements, with an overlap of 126 kb, are located 230 kb upstream of FOXL2, telomeric to the reported translocation breakpoints. Moreover, the shortest region of deletion overlap (SRO) contains several conserved nongenic sequences (CNGs) harboring putative transcription-factor binding sites and representing potential long-range cis-regulatory elements. Interestingly, the human region orthologous to the 12-kb sequence deleted in the polled intersex syndrome in goat, which is an animal model for BPES, is contained in this SRO, providing evidence of human-goat conservation of FOXL2 expression and of the mutational mechanism. Surprisingly, in a fifth family with BPES, one rearrangement was found downstream of FOXL2. In addition, we report nine novel rearrangements encompassing FOXL2 that range from partial gene deletions to submicroscopic deletions. Overall, genomic rearrangements encompassing or outside of FOXL2 account for 16% of all molecular defects found in our families with BPES. In summary, this is the first report of extragenic deletions in BPES, providing further evidence of potential long-range cis-regulatory elements regulating FOXL2 expression. It contributes to the enlarging group of developmental diseases caused by defective distant regulation of gene expression. Finally, we demonstrate that CNGs are candidate regions for genomic rearrangements in developmental genes.

Human herpesvirus 6 (HHV-6) is neurophilic, and its relationship with Alzheimer’s disease (AD) remains controversial. This study aimed to examine the relationships between HHV-6 and cognitive abilities in elderly people aged 60 years or above from communities in Shenzhen. We recruited participants from 10 community health service centers in Shenzhen. Participants were divided into case and control groups according to Mini-Mental State Examination (MMSE) scale standards and were included in this study with 1:1 matching based on sex and age (± 3 years). The HHV-6 gene was detected by real-time fluorescent quantitative PCR, and the HHV-6 copy number was quantified. A total of 580 participants (cases, n = 290; controls, n = 290), matched for gender and age was included in this study. A positive HHV-6 test was not associated with a significant difference in global cognitive performance (ORadjusted = 1.651, 95

Active and passive exposure to tobacco smoke may increase risk of cognitive decline. However, effects of enhanced the aging process on the association of urinary nicotine metabolites with cognitive impairment remain unclear. In this study, 6657 Chinese older adults completed the physical examinations and cognitive tests. We measured urinary nicotine metabolite levels, mitochondrial DNA copy number (mtDNA-CN), and relative telomere length (RTL) and analyzed effects of urinary nicotine metabolites and their interaction with mtDNA-CN or RTL on cognitive impairment by generalized linear models and qg-computation, respectively. Each 1-unit increase in urinary 3-OHCot, 3-OHCotGluc, CotGluc, or NicGluc levels corresponded to a 1.05-, 1.09-, 1.04-, and 0.90-fold increased risk of cognitive impairment. Each 1-quantile increment in the mixture level of 8 nicotine metabolites corresponded to an increment of 1.40- and 1.34-fold risk of cognitive impairment in individuals with longer RTL or low mtDNA-CN. Urinary 3-OHCotGluc and RTL or mtDNA-CN exhibited an additive effect on cognitive impairment in addition to the mixture of 8 nicotine metabolites and mtDNA-CN. The findings suggested that aging process may increase the risk of tobacco-related cognitive impairment.

Abstract Background: Previous studies have suggested a correlation between alterations in the routine blood check markers and cognitive impairment. Objective: We aimed to explore the relationship between routine blood parameters and cognitive impairment. Methods: In this retrospective case-control study, 8,025 people over 60 years of age were enrolled from 51 community health centers in Luohu District of Shenzhen City from 2017 to 2018. According to the mini-mental state examination (MMSE) score and educational level, participants were divided into a cognitive impairment group (n=385) and normal cognitive function group (n=7,640). Nonparametric test, chi-square test, and binary logistic regression were applied to analyze the data. Results: Compared to the normal cognitive function group, the lymphocyte-to-monocyte ratio (LMR), packed-cell volume (PCV), and platelet count (PLT) in the cognitive impairment group were significantly lower (7.26 [5.50,8.81] vs. 7.45 [5.80,9.35]; 40.1 [36.65,42.95] vs. 40.5 [37.7,43.1]; 216 [190,258] vs. 228 [196,261], p<0.05, respectively), while the monocyte count and mean corpuscular hemoglobin concentration (MCHC) were higher (0.31 [0.25, 0.38] vs. 0.3 [0.24, 0.37]; 336 [330, 343] vs. 335 [328, 342], p<0.05, respectively). Additionally, MCHC [odds ratio (OR):1.011, 95% confidence interval (CI) :1.001–1.021, p = 0.033] and PCV [OR: 0.993, 95% CI: 0.987–0.999, p = 0.033) were independently associated with cognitive impairment. Conclusion: The alterations in some routine blood check parameters, including reduced LMR, PCV, and PLT, and elevated monocyte count and MCHC, may be associated with cognitive impairment.