Experimental gerontology最新文献

Objectives

This systematic review with meta-analysis aimed to evaluate the effects of elastic band training (EBT) on body composition and physical performance in apparently healthy older people.

Methods

A systematic literature search was conducted between October 2023 and May 2024 using the core collection of six generic databases: PubMed, ProQuest, EBSCOhost, CINAHL Complete, Scopus, and Web of Science. The PRISMA, TESTEX, RoB 2, and GRADE tools assessed the evidence's methodological quality and certainty. The protocol was registered in PROSPERO (code: CRD42024547050).

Results

Of 5916 records, 9 randomized and non-randomized controlled trials involving 477 healthy older people were included. Six meta-analyses were performed showing significant improvements in 30-second chair stand (SMD = 3.03; 95 % CI = 0.14 to 5.93; I² = 100 %; p = 0.04), sit-and-reach (SMD = 2.09; 95 % CI = 0.15 to 4.03; I² = 100 %; p = 0.04) and timed up-and-go (SMD = 3.10; 95 % CI = 1.67 to 4.53; I² = 98 %; p < 0.0001) tests. However, in maximal isometric handgrip strength, back-scratch test, and fat-free mass, no significant improvements (p > 0.05) in favor of EBT were reported.

Conclusion

EBT improves 30-second chair stand, sit-and-reach, and timed up-and-go in older people. Nevertheless, the certainty of evidence is very low; thus, not definitive recommendations can be made.

Age-related physical and cognitive decline may be ameliorated by consuming functional foods. d-Allose, reported to have multiple health benefits, may temper aging phenotypes, particularly brain function. We investigated whether d-allose supplementation improves cognitive function. A standard battery of behavioral tests was administered to 18-month-old male mice after consuming diet containing 3 % d-allose for 6 months. Following a wire-hanging test, an open-field test, Morris water maze, fear-conditioning, and an analgesia test were sequentially performed. Bone density and strength were assessed afterwards. Possible mechanism(s) under-lying memory changes in hippocampus were also examined with a DNA microarray. d-Allose failed to influence muscle strength, locomotor activity and anxiety, fear memory, or pain sensitivity. However, d-allose improved hippocampus-dependent spatial learning and memory, and it may contribute to increase bone strength. d-Allose also changed the expression of some genes in hippocampus involved in cognitive functions. Long-term d-allose supplementation appears to modestly change aging phenotypes and improve spatial memory.

Background

The relationship between serum lipids and sarcopenia remains unclear due to conflicting results in previous studies.

Objective

To explore the associations and potential causality between serum lipids, including high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC), and sarcopenia.

Methods

Data from the National Health and Nutrition Examination Survey (NHANES) were analysed using multivariable regression and restricted cubic splines (RCSs) to assess the associations between serum lipids and sarcopenia. Bidirectional Mendelian randomization (MR) was employed to investigate the causal relationships with sarcopenia-related traits such as appendicular lean mass (ALM), hand grip strength, and usual walking pace.

Results

Serum HDL-C and TG levels were inversely associated with ALMBMI, with each 1-unit increase linked to a 0.13 % and 1.32 % decrease, respectively. Elevated TG, but not HDL-C, LDL-C, or TC levels, was significantly associated with an increased risk of sarcopenia (P for trend = 0.001). RCS analysis revealed a log-shaped dose-response relationship between TG and sarcopenia risk (P overall <0.001, P non-linear <0.001), with a cutoff value of 92.75 mg/dL. Genetically predicted HDL-C, LDL-C, and TG were associated with ALM. Conversely, ALM showed an inverse causal relationship with all four serum lipids. Additionally, genetically predicted usual walking pace influenced HDL-C and TG levels (P < 0.001).

Conclusion

The study reveals a nonlinear association between TG levels and sarcopenia risk, and a bidirectional association between lipid profiles and muscle mass, underscoring the need for further research to elucidate these mechanisms.

Aim

The aim of this study was to evaluate the potential protective effect of Qiju Granule in a rat model of age-related macular degeneration (AMD) and investigate the underlying mechanisms involved.

Methods

Rats were injected intravenously with 40 mg/kg of sodium iodate (SI) to induce a dry AMD model. The rats in the treatment group received three different doses of Qiju Granule once a day via gavage, while the rats in the control group were given an equal volume of physiological saline. On day 14 and day 28 following the intervention, various methods were employed to evaluate retinal function and structure, including electroretinography (ERG), optical coherence tomography (OCT), and histological examination. The expression of glial fibrillary acidic protein (GFAP), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), and ciliary neurotrophic factor (CNTF) was assessed via immunofluorescence. Beyond immunofluorescence, the mRNA levels of bFGF, BDNF, and CNTF were quantitatively determined using real-time polymerase chain reaction (qRT-PCR).

Results

Rats treated with Qiju Granule exhibited significant improvements in both retinal function and structure compared to the model group. The most noteworthy effects were observed at a high dose of Qiju Granule. Furthermore, the expression levels of bFGF, BDNF, and CNTF were significantly unregulated in the treated groups compared to the model group.

Conclusions

Qiju Granule demonstrated a protective effect on the retina in the SI-induced rat model of AMD. The protective mechanism may be attributed to the upregulation of retinal neurotrophic factors expression.

Obsessive-compulsive disorder (OCD) is a prevalent mental condition characterized by recurrent, unwanted thoughts (obsessions) and repetitive behaviors (compulsions), significantly disrupting daily functioning and social interactions. Transcranial direct current stimulation (tDCS) presents a promising non-invasive treatment modality aimed at alleviating symptoms. However, the evidence regarding its effectiveness remains inconclusive. This study seeks to address this gap by conducting a systematic review and meta-analysis of clinical trials, offering improved guidance for clinical intervention. A comprehensive search strategy was implemented across multiple databases, including PubMed, Cochrane CENTRAL, Embase, Scopus, and Web of Science. This search focused strictly on randomized controlled trials (RCTs) involving 147 patients. These trials evaluated the efficacy of tDCS in OCD patients. Subsequent data extraction, risk of bias assessment, and statistical analysis using Review Manager software revealed the potential efficacy of tDCS in reducing OCD symptoms. The meta-analysis not only fails to demonstrate significant superiority of active tDCS over sham tDCS but also suggests that sham tDCS may be more effective than active tDCS in reducing OCD symptoms. This finding diminishes the promise of tDCS as an effective treatment for OCD. Larger trials are warranted to further elucidate these findings.

Background

Parkinson's disease (PD) is a common central neurodegenerative disease in middle-aged and elderly people. The progressive degeneration and death of dopaminergic neurons leads to insufficient dopamine (DA) neurotransmitters. Acupuncture and moxibustion can alleviate the aging of neurons. Therefore, studying the neuroprotective effects of electroacupuncture (EA) in PD mice is particularly important.

Methods

Intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg) was used to establish a PD mouse model, and lipopolysaccharide (LPS) was used to induce microglia polarization. Western blotting, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), Nissl staining and immunohistochemistry were used to detect neuronal apoptosis and injury, α-syn expression and microglial accumulation in PD mice. In addition, the levels of inflammatory factors were determined using enzyme-linked immunosorbent assay (ELISA). Flow cytometry was used to detect the Ca²⁺ content. The fluorescein isothiocyanate (FITC) labeling method was used to assess glucose uptake. A reagent kit was used to detect glucose and lactate levels.

Results

MPTP induced the selective loss of DA neurons in the SN of mice, altered Ca²⁺ homeostasis, and induced an inflammatory response. In addition, maintaining Ca²⁺ homeostasis depends on the activity of transient receptor potential channel 1 (TRPC1). EA therapy promotes TRPC1 expression, which has a negative regulatory effect on sodium–glucose cotransporter 1 (SGLT1). Under the action of EA, TRPC1 protein expression increased, Ca²⁺ concentrations increased, and the effect of SGLT1 was inhibited, thereby facilitating glucose metabolism, blocking the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway, restraining M1 polarization of microglia, and alleviating the PD process.

Conclusion

EA promotes TRPC1/Ca²⁺ pathway activation, inhibits SGLT1-mediated regulation of glucose metabolism and PI3K/AKT pathway activation, inhibits microglial M1 polarization, and alleviates PD.

Objective

A considerable percentage of individuals with chronic kidney disease (CKD) are reported to be frail. Lower physical activity and higher sedentary time are most consistently associated with frailty among the potentially alterable risk factors. Although the single effect of physical activity or sedentary time on suppressing frailty have been widely studied, whether physical activity can mitigate or counteract the detrimental consequences of higher sedentary time on frailty among CKD population has never been explored. This study aims to explore whether and to what extent the correlation between sedentary time and frailty was diminished by physical activity among CKD population.

Study design and setting

Data were acquired from the National Health and Nutrition Examination Survey (NHANES) 2007 to 2018 cycles. Frailty index was assessed using 49-item deficit model. Physical activity and sedentary time were measured using the Global Activity Questionnaire. Weighted binary logistic regression models, restricted cubic spline models and sensitivity analyses were performed to investigate the aforementioned relationship.

Results

The final sample included 2551 adults aged ≥20 years with CKD, which is represented a weighted number of 4.98 million noninstitutionalized US population. In the fully adjusted model, the group with low physical activity was 1.56 (95 % CI:1.19, 2.03) times more likely to develop frailty than the group with high physical activity and each unit of increase of sedentary time was associated with an 41 % increased risk of frailty (OR = 1.41, 95 % CI = 1.04–1.89). Our findings also indicated that engaging in 1240–6200 MET-min/week of high physical activity was associated with a decreased risk of frailty related to moderate-to-high sedentary time among CKD population (OR = 0.69, 95 % CI = 0.49–0.99, P = 0.044). In subgroup analyses, high physical activity was associated with a 0.43-fold (95%CI: 0.24, 0.77) decreased risk of moderate-to-high sedentary time associated with frailty in female groups and a significant modification effect of gender was uncovered (P_interaction = 0.024).

Conclusion

High physical activity was associated with a decreased risk of frailty related to moderate-to-high sedentary time in adults with CKD, especially in females subgroups.

Background

While patients affected by mild cognitive impairment (MCI) exhibit characteristic voxel-mirrored homotopic connectivity (VMHC) alterations, the ability of such VMHC abnormalities to predict the diagnosis of MCI in these patients remains uncertain. As such, this study was performed to evaluate the potential role of VMHC abnormalities in the diagnosis of MCI.

Methods

MCI patients and healthy controls (HCs) were enrolled and subjected to resting-state functional magnetic resonance imaging (rs-fMRI) and neuropsychological testing. VMHC and support vector machine (SVM) techniques were then used to examine the collected imaging data.

Results

Totally, 53 MCI patients and 68 healthy controls were recruited. Compared to HCs, MCI patients presented with an increase in postcentral gyrus VMHC. SVM classification demonstrated the ability of postcentral gyrus VMHC values to classify HCs and MCI patients with accuracy, sensitivity, and specificity values of 63.64 %, 71.69 %, and 89.71 %, respectively.

Conclusion

VMHC abnormalities in the postcentral gyrus may be mechanistically involved in the pathophysiological progression of MCI patients, and these abnormal VMHC patterns may also offer utility as a neuroimaging biomarker for MCI patient diagnosis.

Introduction

Cyclophosphamide (CP), which is a commonly used chemotherapy drug, can lead to a range of side effects such as immunosuppression, bone marrow suppression, leukopenia, and oxidative stress. This study aims to explore the effects of Auraptene (AUR), which has immunomodulatory and antioxidant properties, on immune function in mice that are experiencing suppression induced by CP.

Materials and methods

The experiment involved 60 male BALB/c mice that underwent a 10-day treatment. On days 1, 3, and 9, CP was given at 80 mg/kg IP doses to induce immunosuppression. The mice were divided into five groups: Control group, CP group, CP + liposomal AUR 0.2 mg/kg (AUR 0.2), CP + liposomal AUR 0.25 mg/kg (AUR 0.25), and liposomal vehicle group. Various parameters were measured, including mouse weight, immune organ weight index (spleen and thymus), spleen and thymus histopathology, levels of inflammatory cytokines (IL2, IL10, IL4, IFN-γ), TH1/TH2 balance ratio, IgG and IgM immunoglobulin levels, white blood cell count, platelets, neutrophils, lymphocytes, and oxidative activity measured by MDA, SOD, and Total Antioxidant.

Results

In the group treated with CP, the mice showed a significant decrease in weight compared to the control group. In contrast, the group treated with AUR maintained their weight and did not show a significant difference from the control group. AUR 0.25 reduced the damage to the spleen and thymus caused by CP. Additionally, AUR 0.25 demonstrated a significant decrease in IL4 and IL10 levels compared to the CP group (p = 0.04), approaching the levels of the control group. Furthermore, IL2 and IFN-γ levels in the AUR 0.25 group significantly increased (p = 0.04) compared to the CP group, reaching levels similar to the control group. AUR also increased serum IgM and IgG levels two to three times compared to the CP group, approaching the levels of the control group. MDA levels in the AUR 0.25 group decreased to normal and control levels. AUR 0.25 also showed increased SOD and Total Antioxidant levels. Additionally, white blood cells, platelets, neutrophils, and lymphocytes in the AUR group significantly increased compared to the CP group, reaching normal levels similar to the control group. The TH1/TH2 ratio in the AUR group exhibited a significant increase of two and a half times (p = 0.002) compared to the CP group.

Conclusion

These results show that AUR protects against the side effects of CP by increasing the function of the humoral and cellular immune system through the balance of TH1/TH2 and increasing the level of immunoglobulins, as well as increasing the antioxidant activity and the protective role of cytotoxicity.

Skin, as the outermost protective barrier of the body, becomes damaged with age and exposure to external stimuli. Dermal fibroblasts age and undergo apoptosis, which decreases collagen, collagen fibers, elastic fibers, hyaluronic acid, etc., leading skin to loss of elasticity and appearance of wrinkles. Skin aging is complex, involving several biological reactions，and various treatment methods are used to treat it. This review focuses on the importance of autophagy and cell proliferation in skin anti-aging, summarizes research progress on skin anti-aging by regulating autophagy and promoting the proliferation of dermal fibroblasts, and discusses future directions on skin anti-aging research.