One of the fastest-growing malignant tumors in the world is thyroid cancer (TC), and there are currently no effective treatments for its aggressive subtypes, such as anaplastic carcinoma and radioactive iodine-refractory differentiated thyroid carcinoma. Recent investigations have shown that DNA methylation and metabolic reprogramming are not independent events, but rather create a closely interconnected, mutually reinforcing network of carcinogenic processes. On the one hand, metabolic reprogramming influences the methylation status of tumor suppressor genes and thyroid function genes by dynamically regulating the activity of DNA methyltransferases and demethylases through important metabolites (such as S-adenosylmethionine, or SAM, and α-KG) and oncogenic signaling pathways (like PI3K/AKT). Conversely, DNA methylation systematically remodels cellular glucose, lipid, and amino acid metabolism by directly silencing metabolic enzyme genes (such as FASN and GLS) and thyroid differentiation markers (such as NIS) to fulfill its proliferative demands. Tumor growth, treatment resistance, and the development of an immunosuppressive microenvironment are all fueled by this ongoing bidirectional interaction, which creates a self-reinforcing oncogenic cycle. As a result, the limitations of earlier discrete debates on DNA methylation or metabolic reprogramming are overcome in this review. To methodically clarify their crosstalk mechanisms, a theoretical framework based on the “DNA methylation-metabolism axis” is suggested. Additionally, it suggests multimodal therapy approaches that focus on this axis. Incorporating biomimetic delivery technologies, combined with epigenetic, metabolic, and immunotherapies, to lay the groundwork for comprehending TC causes and creating targeted treatments.

Increased entropy is a common cause of disease and aging. Lifespan entropy is the overall increase in disorder caused by a person over their lifetime. Aging leads to the excessive production of reactive oxygen species (ROS), which damage the antioxidant system and disrupt redox balance. Organ aging causes chronic inflammation, disrupting the balance of proinflammatory and anti-inflammatory factors. Inflammaging, which is a chronic low-grade inflammatory state, is activated by oxidative stress and can lead to immune system senescence. During this process, entropy increases significantly as the body transitions from a state of low order to high disorder. However, the connection among inflammation, aging, and immune system activity is still not fully understood. This review introduces the idea of the ROS-inflammation-immune balance for the first time and suggests that this balance may be connected to aging and the development of age-related diseases. We also explored how the balance of these three factors controls and affects age-related diseases. Moreover, imbalance in the relationship described above disrupts the regular structures of cells and alters their functions, leading to cellular damage and the emergence of a disorganized state marked by increased entropy. Maintaining a low entropy state is crucial for preventing and reversing aging processes. Consequently, we examined the current preclinical evidence for antiaging medications that target this balance. Ultimately, comprehending the intricate relationships between these three factors and the risk of age-related diseases in organisms will aid in the development of clinical interventions that promote long-term health.

The global surge in the population of people 60 years and older, including that in China, challenges healthcare systems with rising age‐related diseases. To address this demographic change, the Aging Biomarker Consortium (ABC) has launched the X-Age Project to develop a comprehensive aging evaluation system tailored to the Chinese population. Our goal is to identify robust biomarkers and construct composite aging clocks that capture biological age, defined as an individual’s physiological and molecular state, across diverse Chinese cohorts. This Perspective outlines the core objectives, methodological framework and key deliverables of the X-Age Project, including cohort recruitment, standardized sample collection, multimodal data acquisition and clock model development. By integrating interdisciplinary expertise, we aim to provide a practical and scalable platform for understanding aging complexity and heterogeneity, early detection of accelerated aging and evaluation of aging interventions. In this Perspective, members of the Aging Biomarker Consortium outline the X-Age Project, an Aging Biomarker Consortium plan for building standardized aging clocks in China. The authors discuss the project roadmap and its aims of decoding aging heterogeneity, detecting accelerated aging early and evaluating geroprotective interventions.

Background: Thyroid function differs between the oldest-old and younger adults, however, there is a lack of appropriate RIs for the serum FT4, T4, FT3, T3, and TSH concentrations for the oldest-old. Methods: A total of 349 people was selected from the natural longevity cohort of Guangxi residents over 90 years old. The distributions of serum FT4, T4, FT3, T3, and TSH concentrations and the FT3/FT4 ratio were also analyzed. Regression curves and centile curves were constructed. Correlations between body indices and blood pressure and serum thyroid-related hormone levels were analyzed. The RIs were determined using a nonparametric approach (2.5th-97.5th percentiles) following the CLSI guidelines. Results: The RIs for Chinese oldest-old are different from the current standard RIs for younger adults. A notable correlation was found between FT4 levels and age. BMI and WHtR were positively correlated with FT4, FT3, T3 and the FT3/FT4 ratio. The T3 level is correlated with SBP and DBP, and the FT3/FT4 ratio is correlated with SBP. The RIs established for the healthy oldest-old were as follows: T4, 81-193 nmol/L; FT4, 10.39-20.46 pmol/L; T3, 0.94-2.05 nmol/L; FT3, 3.56-6.43 pmol/L; TSH, 0.29-5.28 μIU/ml; and FT3/FT4, 0.197-0.496. Conclusions: In this study, we established RIs of thyroid-related hormone levels for the oldest-old in China and evaluated the associations between thyroid hormone levels and body indices. These findings may provide evidence for the diagnosis and treatment of thyroid-related diseases in the oldest-old.

As effectors of interactions between genes and the environment, plasma proteins can monitor homeostasis and reflect the aging state of an organism. However, biomarkers of aging that are associated with homeostasis are still unclear. This study investigates the phenotype-related plasma proteome profiles of healthy individuals and to identify proteins that are specifically related to aging and physiological indices and their expression patterns across the lifespan. From September 2020 to March 2021, 71 participants aged over 20 to 100 years were enrolled in this cross-sectional study. Data were analyzed from April 2021 to December 2023. The plasma proteome was analyzed to identify proteins that are specifically related to aging and their expression patterns across the lifespan. Then, hub proteins were screened through correlation of aging proteins with physiological and biochemical phenotypes. Based on levels of plasma proteins, physiological indices are associated with age. Additionally, these differences in protein expression correlate with age and physiological indices. Finally, we identified 20 hub proteins that correlate with both physiological indices and age, and these proteins are involved in oxidative stress, inflammation and metabolism. Bibliometric analysis confirmed that 8 hub proteins (CD44, CD14, IGF2, CFD, LBP, IGFBP3, EFEMP1, and AHSG) associated with age affect organ function by mediating homeostasis. Plasma proteins associated with both age and physiological indices are involved in oxidative stress, inflammation, and metabolism. This is the first investigation to link aging and homeostasis based on plasma proteins.

Purpose: The aim of this study was to establish reference intervals for serum TSH, T4, FT4, T3, and FT3 concentrations and the FT3/FT4 ratio in a longevous population and to determine the relationships between thyroid-related hormones and body indices in Guangxi, China.Material and Methods: A total of 349 people were selected from the natural longevity cohort of Guangxi residents over 90 years old. Blood specimens from participants were collected by standard procedures, and the serum FT4, T4, FT3, T3 and TSH concentrations of each participant were analyzed via the Roche Cobas system. The distributions of serum FT4, T4, FT3, T3, and TSH concentrations and the FT3/FT4 ratio were also analyzed. Regression curves and centile curves were constructed. Correlations between body indices and blood pressure and serum thyroid-related hormone levels were analyzed. The RIs were calculated using a nonparametric method (2.5th–97.5th percentiles) according to the CLSI guidelines. The RIs for FT4, T4, FT3, T3 and TSH among this population were compared with the standard RIs for adults in China.Results: The RIs for longevous populations are different from the current standard RIs for adults. There was a significant correlation between FT4 and age. BMI and WHtR were positively correlated with FT4, FT3, T3 and the FT3/FT4 ratio. The T3 level is correlated with SBP and DBP, and the FT3/FT4 ratio is correlated with SBP. The RIs established for the healthy longevous population were as follows: T4, 81-193 nmol/L; FT4, 10.39-20.46 pmol/L; T3, 0.94-2.05 nmol/L; FT3, 3.56-6.43 pmol/L; TSH, 0.29-5.28 μIU/ml; and FT3/FT4, 0.197-0.496.Conclusions: We established a panel of scientific and reasonable RIs of thyroid-related hormone levels for the longevous population in China and evaluated the associations between thyroid hormone levels and body indices. These findings could guide the diagnosis and treatment of senile thyroid-related diseases.Funding: This work was supported by National Key R&D Program of China (2018YFC2000400), Natural Science Foundation of China (81870552, 81400790).Declaration of Interest: The authors declare that they have no competing interests.Ethical Approval: This study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the Ethics Committee of Beijing Hospital (2019BJYYEC-118-02). Informed consent was obtained from the subjects or their legally authorized representative.

Background and aims: Although the life expectancy of women systematically and robustly exceeds that of men, specific differences and molecular mechanisms of sex in influencing longevity phenotypes remain largely unknown. Therefore, we performed transcriptome sequencing of peripheral blood samples to explore regulatory mechanisms of healthy longevity by incorporating sex data. Methods: We selected 34 exceptional longevity (age: 98.26 +/- 2.45 years) and 16 controls (age: 52.81 +/- 9.78) without advanced outcomes from 1363 longevity and 692 controls recruited from Nanning of Guangxi for RNA sequencing 1. The transcriptome sequencing 1 data of 50 samples were compared by longevity and sex to screen differentially expressed genes (DEGs). Then, 121 aging samples (40-110 years old) without advanced outcomes from 355 longevity and 294 controls recruited from Dongxing of Guangxi were selected for RNA sequencing 2. The genes associated with aging from the transcriptome sequencing 2 of 121 aging samples were filtered out. Finally, the gender-related longevity candidate genes and their possible metabolic pathways were verified by cell model of aging and a real-time polymerase chain reaction (RT-PCR). Results: Metabolism differs between male and female and plays a key role in longevity. Moreover, the principal findings of this study revealed a novel key gene, UGT2B11, that plays an important role in regulating lipid metabolism through the peroxisome proliferator activated receptor gamma (PPARG) signalling pathway and ultimately improving lifespan, particularly in females. Conclusion: The findings suggest specific differences in metabolism affecting exceptional longevity phenotypes between the sexes and offer novel therapeutic targets to extend lifespan by regulating lipid homeostasis.

For thousands of years, traditional natural medicine has been well documented to have low toxicity and good curative effects; however, the bioactive molecules and molecular mechanisms are unclear in many cases due to the difficulties in identifying pharmacodynamic molecules. Here, we report the successful identification of a novel active molecule, CPB13, with antiapoptotic functions from a natural drug (Colla corii asini, CCA) by combining phenotypic screening with proteomics approaches. Functional studies in cell and animal models demonstrated that the molecule CBP13 improves the morphology and functions of mitochondria in a dose-dependent manner and inhibits mitochondrial protein reduction and apoptosome activity. Molecular modeling and docking analysis revealed that CBP13 prefers a concave conformation, which can potentially bind to human cytochrome C and Apaf-1, providing hints regarding the molecular basis by which CBP13 inhibits the apoptosis signaling cascade. The results indicate that CBP13 can be developed into drugs that regulate apoptosis, providing a new avenue for antiaging and anti-inflammatory applications.

Objective: Senior citizens suffering from cognitive impairment (CI) are on the East Asia rise. Multiple variables could lead to inter-/intra-individual cognition effectiveness variations, though previous research efforts did not consider weighting issues. Methods: This study scrutinized 5639 participants meeting required inclusion criteria by the CHARLS. Cognitive capacity was evaluated through Mini-Mental State Examination (MMSE). Considering that MMSE scorings were not following normal distribution, a non-parametric test and multiple linear regression were performed to screen candidate variables linked to cognitive capacity. Such applicability of candidate factors in the cumulative effect and the weighting of the impact on cognitive performance were evaluated by random forest (RF) algorithm. Results: Age, gender, education, marital status, residence, the type of residence, exercise, socialization level and drinking were correlated to MMSE scorings (p < 0.05). Among them, age, education, gender and sociality were correlated to individual MMSE items (p < 0.05). Regardless of MMSE scores and several MMSE items, age is always a prime factor. However, in the attention and computation item, education is better than age and ranks first. Conclusions: This preliminary study prompted age, education, gender, and sociality with varying weightings to be linked to cognitive capacity within a Chinese cohort by differing cognitive aspects. At different levels of cognitive performance, the main risk factors are basically similar, but there are still some differences.

It is long observed that females tend to live longer than males in nearly every country. However, the underlying mechanism remains elusive. In this study, we discovered that genetic associations with longevity are on average stronger in females than in males through bio-demographic analyses of genome-wide association studies (GWAS) dataset of 2178 centenarians and 2299 middle-age controls of Chinese Longitudinal Healthy Longevity Study (CLHLS). This discovery is replicated across North and South regions of China, and is further confirmed by North-South discovery/replication analyses of different and independent datasets of Chinese healthy aging candidate genes with CLHLS participants who are not in CLHLS GWAS, including 2972 centenarians and 1992 middle-age controls. Our polygenic risk score analyses of eight exclusive groups of sex-specific genes, analyses of sex-specific and not-sex-specific individual genes, and Genome-wide Complex Trait Analysis using all SNPs all reconfirm that genetic associations with longevity are on average stronger in females than in males. Our discovery/replication analyses are based on genetic datasets of in total 5150 centenarians and compatible middle-age controls, which comprises the worldwide largest sample of centenarians. The present study's findings may partially explain the well-known male-female health-survival paradox and suggest that genetic variants may be associated with different reactions between males and females to the same vaccine, drug treatment and/or nutritional intervention. Thus, our findings provide evidence to steer away from traditional view that “one-size-fits-all” for clinical interventions, and to consider sex differences for improving healthcare efficiency. We suggest future investigations focusing on effects of interactions between sex-specific genetic variants and environment on longevity as well as biological function.

The accumulation of senescent cells can lead to tissue degeneration, chronic inflammatory disease and age-related tumorigenesis. Interventions such as senolytics are currently limited by off-target toxicity, which could be circumvented by instead enhancing immune-mediated senescent cell clearance; however, immune surveillance of senescent cells is often impeded by immunosuppressive factors in the inflammatory microenvironment. Here, we employ a chimeric peptide as a ‘matchmaker’ to bind to the urokinase-type plasminogen activator receptor, a cell surface marker of senescent cells. This peptide modifies the cell surface with polyglutamic acid, promoting immune cell-mediated responses through glutamate recognition. By enhancing the recruitment of immune cells and directly coupling senescent cells and immune cells, we show that this chimeric peptide induces immune clearance of senescent cells and restores tissue homeostasis in conditions such as liver fibrosis, lung injury, cancer and natural aging in mice. This chimeric peptide introduces an immunological conversion strategy that rebalances the senescent immune microenvironment, offering a promising direction for aging immunotherapy. Ming, Yang, Huang et al. design a chimeric matchmaker peptide, which targets a senescent cell-specific surface marker and modifies the cell surface with polyglutamic acid. This promotes interactions with natural killer cells and senescent cell clearance in liver fibrosis, lung injury, cancer and natural aging.

There is a significant association between the pathogenesis of Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM), in which the blood-brain barrier (BBB), as an essential bridge connecting the periphery to the central nervous system, maybe a vital link in revealing the mechanism of the association between the two diseases. The function of the T2DM blood-brain barrier and its influence on the pathogenesis of AD remains unclear. We found reduced Glut-1 and Claudin-5 immunopositive reactive regions in the brains of spontaneous T2DM cynomolgus monkeys by multiple immunological experiments, suggesting dysfunctional transport and impaired integrity of the blood-brain barrier. Meanwhile, different degrees of AD-like pathology formation were found in the brains of spontaneous T2DM cynomolgus monkeys and were positively correlated with the degree of blood-brain barrier damage. The present study demonstrates that T2DM leads to impairmed of blood-brain barrier integrity, subsequently affecting AD pathogenesis.

International research on healthy life expectancy (HALE) focuses on inequality of socioeconomic status and individual natural attributes. With the acceleration of population ageing and the increase in average life expectancy, the extension of unhealthy life expectancy and the increase of social and economic burden caused by diseases have gradually attracted the attention of countries around the world. Therefore, the evaluation of disease factors affecting HALE is a meaningful direction in the future. This study introduces the development process and commonly used measurement methods of HALE. According to the definition of health from the Global Burden of Disease Study and World Health Organization, physical and mental diseases such as cardiovascular and cerebrovascular diseases, chronic respiratory diseases, diabetes, malignant tumors and depression were selected to summarize the impact of these diseases and pre-disease states on HALE. It is expected to provide a theoretical basis for the formulation of relevant public health policies and the improvement of quality of life in China.

Background The association between fine particular matter (PM2.5) and frailty is less studied, and the national burden of PM2.5-related frailty in China is unknown. Objective To explore the association between PM2.5 exposure and incident frailty in older adults, and estimate the corresponding disease burden. Design Chinese Longitudinal Healthy Longevity Survey from 1998 to 2014. Setting Twenty-three provinces in China. Subjects A total of 25,047 participants aged >= 65-year-old. Methods Cox proportional hazards models were performed to evaluate the association between PM2.5 and frailty in older adults. A method adapted from the Global Burden of Disease Study was used to calculate the PM2.5-related frailty disease burden. Results A total of 5,733 incidents of frailty were observed during 107,814.8 person-years follow-up. A 10 mu g/m(3) increment of PM2.5 was associated with a 5.0% increase in the risk of frailty (Hazard Ratio = 1.05, 95% confidence interval = [1.03-1.07]). Monotonic, but non-linear exposure-response, relationships of PM2.5 with risk of frailty were observed, and slopes were steeper at concentrations >50 mu g/m(3). Considering the interaction between population ageing and mitigation of PM2.5, the PM2.5-related frailty cases were almost unchanged in 2010, 2020 and 2030, with estimations of 664,097, 730,858 and 665,169, respectively. Conclusions This nation-wide prospective cohort study showed a positive association between long-term PM2.5 exposure and frailty incidence. The estimated disease burden indicated that implementing clean air actions may prevent frailty and substantially offset the burden of population ageing worldwide.

Objective: To investigate the relationship between serum lysophosphatidylcholine (LPC) level and the health index of the elderly. Methods: A total of 251 subjects were selected from the 2016 baseline survey of the Yongfu Longevity Cohort in Guangxi Province among whom 66, 63 and 122 were in the young and middle-aged group (≤59 years old), the young group (60-89 years old) and the longevity group (≥90 years old), respectively. Demographic data were collected and related indicators of height, weight, blood pressure and lipid metabolism were measured. The cognitive and physical functions of the elderly were assessed by the results of the simple mental state scale and the daily living activity scale to construct the health index of the elderly. The serum levels of LPC16∶0, LPC18∶0, LPC18∶1 and LPC18∶2 were determined by liquid chromatography-tandem mass spectrometry, and the differences among different ages and health status groups were compared. The logistic regression model was used to analyze the relationship between the serum LPC level and the health index of the elderly. Results: With the increase in age, the proportion of female subjects increased, and the rate of smoking and drinking decreased. BMI, TC, TG, LDL-C, diastolic blood pressure, and the four LPCs levels decreased with the increase of age, and systolic blood pressure levels increased with the increase of age (all P values<0.05). There was no significant difference in HDL-C levels among age groups (P>0.05). With the decline of health status in the elderly, serum levels of LPC16∶0, LPC18∶0, LPC18∶1 and LPC18∶2 showed a downward trend (all P values<0.001). After adjusting for age and gender, only LPC18∶0 was associated with the health status in old age [OR (95%CI): 0.48 (0.25-0.92)]. For every 1 standard deviation (16.87 nmol/L) increase in serum LPC18∶0 concentration, the risk of poor health status in old age decreased by 52%. Conclusion: Serum LPC18∶0 was associated with the health status in old age independent of age and sex.

阿尔茨海默病(Alzheimer's disease,AD)是一种进行性神经退行性疾病,以认知障碍、记忆丧失和功能下降为特征.阿尔茨海默病的病理特征包括β-淀粉样斑块和tau蛋白缠结,这些病理改变最终引起大脑特定区域的退化,包括海马体、内嗅皮层和新皮层,从而导致阿尔茨海默病的特征性临床症状.阿尔茨海默病病理的确切机制仍不完全清楚,尽管学者们对阿尔茨海默病进行了广泛的研究,但仍然没有有效的治疗方法可以减缓或阻止疾病的进展.因此,迫切需要开发新的针对阿尔茨海默病潜在病理生理学治疗策略.环状RNA(Circular RNAs,circRNAs)是一类非编码RNA,在各种生物过程中发挥着重要作用,它们的调节异常与包括阿尔茨海默病在内的多种疾病的发病机制有关.本综述将阐述阿尔茨海默病患者中环状RNA的失调、失调的机制、环状RNA在阿尔茨海默病疾病进展中的潜在作用和诊断、治疗的意义以及未来的研究方向.

Background: A variety of factors, including diet and lifestyle, obesity, physiology, metabolism, hormone levels, psychology, and inflammation, have been associated with longevity. The specific influences of these factors, however, are poorly understood. Here, possible causal relationships between putative modifiable risk factors and longevity are investigated.Methods: A random effects model was used to investigate the association between 25 putative risk factors and longevity. The study population comprised 11,262 long-lived subjects (>= 90 years old, including 3484 individuals >= 99 years old) and 25,483 controls (<= 60 years old), all of European ancestry. The data were obtained from the UK Biobank database. Genetic variations were used as instruments in two-sample Mendelian randomization to reduce bias. The odds ratios for genetically predicted SD unit increases were calculated for each putative risk factor. Egger regression was used to determine possible violations of the Mendelian randomization model.Results: Thirteen potential risk factors showed significant associations with longevity (>= 90th) after correction for multiple testing. These included smoking initiation (OR:1.606; CI: 1.112-2.319) and educational attainment (OR:2.538, CI: 1.685-3.823) in the diet and lifestyle category, systolic and dia-stolic blood pressure (OR per SD increase: 0.518; CI: 0.438-0.614 for SBP and 0.620; CI 0.514-0.748 for DBP) and venous thromboembolism (OR:0.002; CI: 0.000-0.047) in the physiology category, obesity (OR: 0.874; CI: 0.796-0.960), BMI (OR per 1-SD increase: 0.691; CI: 0.628-0.760), and body size at age 10 (OR per 1-SD increase:0.728; CI: 0.595-0.890) in the obesity category, type 2 diabetes (T2D) (OR:0.854; CI: 0.816-0.894), LDL cholesterol (OR per 1-SD increase: 0.743; CI: 0.668-0.826), HDL cholesterol (OR per 1 -SD increase: 1.243; CI: 1.112-1.390), total cholesterol (TC) (OR per 1-SD increase: 0.786; CI: 0.702-0.881), and triglycerides (TG) (OR per 1-SD increase: 0.865; CI: 0.749-0.998) in the metabolism category. Both longevity (>= 90th) and super-longevity (>= 99th), smoking initiation, body size at age 10, BMI, obesity, DBP, SBP, T2D, HDL, LDL, and TC were consistently associated with outcomes. The examination of underlying pathways found that BMI indirectly affected longevity through three pathways, namely, SBP, plasma lipids (HDL/TC/LDL), and T2D (p < 0.05).Conclusion: BMI was found to significantly affect longevity through SBP, plasma lipid (HDL/TC/LDL), and T2D. Future strategies should focus on modifying BMI to improve health and longevity.(c) 2023 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Background: Older individuals tend to develop chronic inflammation. As a commonly used nonspecific inflammatory marker, C-reactive protein (CRP) can predict metabolic syndrome, cardiovascular diseases, etc. However, little is known about CRP levels in longevity people.Objectives: Investigate the distribution and correlates of CRP and provide a reference for the establishment of normal interval values in Chinese longevity people over 90 years of age.Methods: We performed a correlation analysis to evaluate the correlation between CRP levels and longevity based on the basic demographic characteristics, anthropometric measurements and blood data of 4,418 participants in the 2015 China Health and Retirement Longitudinal Study and 636 participants in an ongoing longitudinal study of natural longevity people in Guangxi. On this basis, the CRP reference interval for longevity was explored.Results: The CRP concentration was significantly different among the three age groups, with a median of 3.80 mg/L for those older than 90 years, which was significantly higher than that for those aged 45-64 years (median 1.20 mg/L, p < 0.001) and 65-89 years (median 1.30 mg/L, p < 0.001). Body mass index, waist circumference, the waist-to-height ratio, systolic blood pressure, diastolic blood pressure, and fasting and postprandial blood glucose, triglyceride, total cholesterol and low-density lipoprotein cholesterol levels were positively correlated with CRP levels, while fasting high-density lipoprotein cholesterol was negatively correlated with CRP levels. The CRP reference interval (RI) value in longevity people was 0.25-9.22 mg/L.Conclusion: The concentrations of CRP increased with advancing age, and the CRP reference interval was different between older and younger adults.