The aging process and declining muscle strength and function are known to increase the risk of falls in older adults. The Nintendo Wii Balance Board (NWBB) is a cost-effective and easily accessible alternative to traditional dynamometry for measuring lower limb muscle strength. The study objective was to validate the ability of NWBB to assess lower limb muscle strength and screen the risk of falls in older adults. Ninety community-dwelling elderly women, divided into falling risk and non-falling groups, underwent lower limb muscle strength measurements using NWBB. Moreover, the power index of the sit-to-stand test (PSTS) was calculated from the time to completed Five Times Sit-to-Stand Test (FTSST) (TSTS). The correlation between each variable was assessed. The cut-off score, sensitivity, and specificity for the NWBB's measurement of lower limb muscular strength was determined using the receiver operating curve (ROC). The falling-risk elderly women showed significantly higher TSTS and significantly lower PSTS and leg muscle strength measured by NWBB than the non-falling risk group (p-value <0.01). A strong negative correlation was observed between TSTS and lower limb muscle strength measured by NWBB (r = - 0.747, p <0.001). The appropriate cut-off score was >79.83 kg to identify non-falling risk older adults with the best sensitivity (90.38 %) and specificity (86.84 %). In conclusion, the NWBB has demonstrated concurrent validity with established measures of lower limb muscle strength, making it a viable option for screening the risk of falls in elderly women populations.
众所周知，衰老过程和肌肉力量和功能的下降会增加老年人跌倒的风险。任天堂Wii平衡板（NWBB）是一种成本效益高，易于使用的替代传统的动态测量下肢肌肉力量。研究目的是验证NWBB评估老年人下肢肌肉力量和筛查跌倒风险的能力。90名社区老年妇女，分为跌倒风险组和非跌倒组，使用NWBB进行下肢肌肉力量测量。此外，从完成五次坐立测试（FTSST） （TSTS）的时间计算坐立测试（PSTS）的功率指数。评估各变量之间的相关性。采用受试者工作曲线（ROC）确定NWBB测量下肢肌力的截止评分、敏感性和特异性。与无跌倒危险组相比，跌倒危险组的TSTS显著升高，NWBB测量的PSTS和腿部肌力显著降低（p值<；0.01）。TSTS与NWBB测量的下肢肌力呈显著负相关（r = - 0.747, p <0.001）。合适的临界值为79.83 kg，以最佳敏感性（90.38%）和特异性（86.84%）识别无跌倒风险的老年人。总之，NWBB已经证明了与下肢肌肉力量的既定测量方法同时有效，使其成为筛查老年妇女跌倒风险的可行选择。
{"title":"Exploring Nintendo Wii Balance Board as a tool to assess lower limb muscle strength for fall risk screening in elderly women","authors":"Weerasak Tapanya, Noppharath Sangkarit, Patchareeya Amput","doi":"10.1016/j.tma.2024.12.002","DOIUrl":"10.1016/j.tma.2024.12.002","url":null,"abstract":"<div><div>The aging process and declining muscle strength and function are known to increase the risk of falls in older adults. The Nintendo Wii Balance Board (NWBB) is a cost-effective and easily accessible alternative to traditional dynamometry for measuring lower limb muscle strength. The study objective was to validate the ability of NWBB to assess lower limb muscle strength and screen the risk of falls in older adults. Ninety community-dwelling elderly women, divided into falling risk and non-falling groups, underwent lower limb muscle strength measurements using NWBB. Moreover, the power index of the sit-to-stand test (P<sub>STS</sub>) was calculated from the time to completed Five Times Sit-to-Stand Test (FTSST) (T<sub>STS</sub>). The correlation between each variable was assessed. The cut-off score, sensitivity, and specificity for the NWBB's measurement of lower limb muscular strength was determined using the receiver operating curve (ROC). The falling-risk elderly women showed significantly higher T<sub>STS</sub> and significantly lower P<sub>STS</sub> and leg muscle strength measured by NWBB than the non-falling risk group (p-value <0.01). A strong negative correlation was observed between T<sub>STS</sub> and lower limb muscle strength measured by NWBB (r = - 0.747, p <0.001). The appropriate cut-off score was >79.83 kg to identify non-falling risk older adults with the best sensitivity (90.38 %) and specificity (86.84 %). In conclusion, the NWBB has demonstrated concurrent validity with established measures of lower limb muscle strength, making it a viable option for screening the risk of falls in elderly women populations.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 1-8"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143139174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2025.08.002
Joel Cassar , Daniel Kam Yin Chan , Sandro Sperandei , Renfen Chen
Although small vessel vascular dementia (SmVD) remains a significant contributor to global disease burden, its aetiology and pathogenesis are not fully understood. Past research has highlighted an association of SmVD with blood-brain barrier (BBB) dysfunction and neuroinflammation. Studies of claudin-1 polymorphisms and serum cytokines have been found to be useful biomarkers and offer possible mechanistic relationship. However, the pathophysiology and primary factors that contribute to the development and onset of SmVD remain to be further elucidated. This study aimed to evaluate the association of these biomarkers with SmVD through the construction of a logistic regression model. Two datasets from a study group, sourced from the publications of “Association of genetic polymorphisms of claudin-1 with small vessel VD” and “Macrophage and microglia related chemokines are associated with small vessel (white matter) VD: A case-control study”, were merged with multiple imputation chain equations to allow for the construction of a unified logistic regression model. The model incorporated an L2 regularisation penalty to improve the interpretability of the findings. The results showed a significant link between disease comorbidities and SmVD, particularly those with a history of stroke and Parkinson's diseases, while cytokines displayed a weaker association with SmVD. Overall, this study supported the mechanistic theories linking SmVD with BBB dysfunction and neuroinflammation.
{"title":"Predictive model of small vessel vascular dementia based on comorbidities, cytokines and claudin-1 genetic polymorphisms","authors":"Joel Cassar , Daniel Kam Yin Chan , Sandro Sperandei , Renfen Chen","doi":"10.1016/j.tma.2025.08.002","DOIUrl":"10.1016/j.tma.2025.08.002","url":null,"abstract":"<div><div>Although small vessel vascular dementia (SmVD) remains a significant contributor to global disease burden, its aetiology and pathogenesis are not fully understood. Past research has highlighted an association of SmVD with blood-brain barrier (BBB) dysfunction and neuroinflammation. Studies of claudin-1 polymorphisms and serum cytokines have been found to be useful biomarkers and offer possible mechanistic relationship. However, the pathophysiology and primary factors that contribute to the development and onset of SmVD remain to be further elucidated. This study aimed to evaluate the association of these biomarkers with SmVD through the construction of a logistic regression model. Two datasets from a study group, sourced from the publications of “<em>Association of genetic polymorphisms of claudin-1 with small vessel VD”</em> and “<em>Macrophage and microglia related chemokines are associated with small vessel (white matter) VD: A case-control study</em>”, were merged with multiple imputation chain equations to allow for the construction of a unified logistic regression model. The model incorporated an L2 regularisation penalty to improve the interpretability of the findings. The results showed a significant link between disease comorbidities and SmVD, particularly those with a history of stroke and Parkinson's diseases, while cytokines displayed a weaker association with SmVD. Overall, this study supported the mechanistic theories linking SmVD with BBB dysfunction and neuroinflammation.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 66-73"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The hypothesis that metabolic rate (MR) is inversely correlated with lifespan has long been debating. Another area of controversy is the relationship between MR and time-flow perception (TFP), and aging. Objectives: to study the impact of overweight and excess food intake on MR, TFP, chronic diseases, aging, lifespan.
Methods
Design: a systematic review. Settings: Web of Science, Scopus, Science Direct, Kopernio, PubMed, and Mendeley were searched for articles published for 44 years (1979–2022). The study bases on a systematic literature review of 3612 articles published worldwide.
Results
In total, 107 full-text articles were assessed for eligibility. Overweight/overeating accelerates MR, leading to a hyper-metabolic mode of the body. MR and lifespan are inversely correlated. TFP depends on MR; accelerated MR provides TFP deceleration.
Every person has an individual ability to gain weight up to ‘maximum bodyweight’, which indicates the individual potential energy for weight gain. Overweight excessively consumes the body's ‘vital energy’, and devours the body potential energy. Weight loss creates ‘body potential power to weight gain’ that increases physical/mental activity, recovers from disease, or weight regain. The body should consume fewer calories due the decline in MR with age.
Conclusions
Our findings support that overweight and overeating increase in MR, which delays time-flow perception, accelerates aging, and limits lifespan. Metabolic intoxication should be managed during weight loss.
{"title":"Overweight effects on metabolic rate, time perception, diseases, aging, and lifespan: A systematic review with meta-regression analysis","authors":"Kuat Oshakbayev , Aigul Durmanova , Altay Nabiyev , Antonio Sarria-Santamera , Alisher Idrissov , Gulnara Bedelbayeva , Abduzhappar Gaipov , Ayan Mitra , Meruyert Gazaliyeva , Bibazhar Dukenbayeva , Gani Kuttymuratov","doi":"10.1016/j.tma.2024.12.001","DOIUrl":"10.1016/j.tma.2024.12.001","url":null,"abstract":"<div><h3>Background</h3><div>The hypothesis that metabolic rate (MR) is inversely correlated with lifespan has long been debating. Another area of controversy is the relationship between MR and time-flow perception (TFP), and aging. Objectives: to study the impact of overweight and excess food intake on MR, TFP, chronic diseases, aging, lifespan.</div></div><div><h3>Methods</h3><div>Design: a systematic review. Settings: Web of Science, Scopus, Science Direct, Kopernio, PubMed, and Mendeley were searched for articles published for 44 years (1979–2022). The study bases on a systematic literature review of 3612 articles published worldwide.</div></div><div><h3>Results</h3><div>In total, 107 full-text articles were assessed for eligibility. Overweight/overeating accelerates MR, leading to a hyper-metabolic mode of the body. MR and lifespan are inversely correlated. TFP depends on MR; accelerated MR provides TFP deceleration.</div><div>Every person has an individual ability to gain weight up to ‘maximum bodyweight’, which indicates the individual potential energy for weight gain. Overweight excessively consumes the body's ‘vital energy’, and devours the body potential energy. Weight loss creates ‘body potential power to weight gain’ that increases physical/mental activity, recovers from disease, or weight regain. The body should consume fewer calories due the decline in MR with age.</div></div><div><h3>Conclusions</h3><div>Our findings support that overweight and overeating increase in MR, which delays time-flow perception, accelerates aging, and limits lifespan. Metabolic intoxication should be managed during weight loss.</div></div><div><h3>Trial registration</h3><div>ClinicalTrials.gov <span><span>NCT06410352</span><svg><path></path></svg></span> (05/08/2024): <span><span>https://register.clinicaltrials.gov/prs/app/action/SelectProtocol?sid&equals;S000EG8K&selectaction&equals;Edit&uid&equals;U0006MBT&ts&equals;56&cx&equals;-vph5l9</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 15-24"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143139475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diabetes management has evolved beyond glycemic control, with emerging evidence demonstrating the multi-system benefits of various anti-diabetic drug classes. This review examines the mechanisms, pharmacokinetics, and therapeutic potential of Glucagon-like Peptide-1 (GLP-1) receptor agonists, Dipeptidyl Peptidase-4 (DPP-4) inhibitors, Sodium- Glucose Cotransporter-2 (SGLT-2) inhibitors, and Thiazolidinediones (TZDs). These agents not only regulate blood glucose but also confer cardiovascular, neuroprotective, renal, and anti-aging effects, positioning them as promising candidates for broader metabolic disorder management. GLP-1 receptor agonists enhance insulin secretion, support weight loss, and exhibit neuroprotective and cardiovascular benefits. DPP-4 inhibitors, which increase endogenous GLP-1 levels, offer stroke prevention and cognitive advantages, particularly in patients with renal impairment. SGLT-2 inhibitors lower blood sugar independently of insulin, reduce heart failure risk, slow kidney disease progression, and possess senolytic properties that may enhance longevity. While TZDs improve insulin sensitivity and beta-cell function, their cardiovascular risks necessitate cautious use. Beyond diabetes, these drugs modulate inflammation, oxidative stress, and metabolic dysfunction—key factors in aging and chronic disease progression. The senolytic potential of SGLT-2 inhibitors, the neurotrophic effects of GLP-1 receptor agonists, and the cardiovascular benefits of DPP-4 inhibitors highlight their broader therapeutic applications. This review underscores a paradigm shift in diabetes management toward a personalized medicine approach. As research advances, integrating these agents into anti-aging and chronic disease prevention strategies may redefine future medical treatments, emphasizing healthier aging and extended lifespan.
{"title":"A comprehensive review of the multisystem benefits of antidiabetic drugs in aging beyond glycemic control","authors":"Fatema-Tuz- Zohora , Sumiya Sharmin Mou , Md Ekramul Haque , Mohana Baidya , Israt Jahan , Md. Elias Al-Mamun","doi":"10.1016/j.tma.2025.08.005","DOIUrl":"10.1016/j.tma.2025.08.005","url":null,"abstract":"<div><div>Diabetes management has evolved beyond glycemic control, with emerging evidence demonstrating the multi-system benefits of various anti-diabetic drug classes. This review examines the mechanisms, pharmacokinetics, and therapeutic potential of Glucagon-like Peptide-1 (GLP-1) receptor agonists, Dipeptidyl Peptidase-4 (DPP-4) inhibitors, Sodium- Glucose Cotransporter-2 (SGLT-2) inhibitors, and Thiazolidinediones (TZDs). These agents not only regulate blood glucose but also confer cardiovascular, neuroprotective, renal, and anti-aging effects, positioning them as promising candidates for broader metabolic disorder management. GLP-1 receptor agonists enhance insulin secretion, support weight loss, and exhibit neuroprotective and cardiovascular benefits. DPP-4 inhibitors, which increase endogenous GLP-1 levels, offer stroke prevention and cognitive advantages, particularly in patients with renal impairment. SGLT-2 inhibitors lower blood sugar independently of insulin, reduce heart failure risk, slow kidney disease progression, and possess senolytic properties that may enhance longevity. While TZDs improve insulin sensitivity and beta-cell function, their cardiovascular risks necessitate cautious use. Beyond diabetes, these drugs modulate inflammation, oxidative stress, and metabolic dysfunction—key factors in aging and chronic disease progression. The senolytic potential of SGLT-2 inhibitors, the neurotrophic effects of GLP-1 receptor agonists, and the cardiovascular benefits of DPP-4 inhibitors highlight their broader therapeutic applications. This review underscores a paradigm shift in diabetes management toward a personalized medicine approach. As research advances, integrating these agents into anti-aging and chronic disease prevention strategies may redefine future medical treatments, emphasizing healthier aging and extended lifespan.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 80-99"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145361988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2025.02.002
Nabanita Ghosh , Krishnendu Sinha
Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the gradual loss of dopaminergic neurons in the substantia nigra, resulting in both motor and non-motor symptoms. A defining feature of PD pathology is the presence of Lewy bodies, which are intracellular inclusions primarily composed of aggregated alpha-synuclein (α-syn) proteins. The abnormal buildup of α-syn, referred to as α-synucleopathy, is a key aspect of PD and other neurodegenerative conditions. Recent research indicates that bacterial amyloids, such as curli proteins produced by Escherichia coli, may influence α-syn aggregation, potentially playing a role in PD development. These discoveries provide a new perspective on the involvement of microbial factors in neurodegenerative diseases, suggesting that curli proteins can cross-seed with α-syn and enhance its aggregation. Understanding these interactions opens up new therapeutic possibilities, including methods to inhibit curli production, prevent curli-α-syn interactions, or target the resulting pathological aggregates. Such therapeutic strategies could offer promising new ways to slow or stop the progression of PD and improve outcomes for patients.
{"title":"Curli protein: A potential contributor to α-synucleopathy in Parkinson's disease","authors":"Nabanita Ghosh , Krishnendu Sinha","doi":"10.1016/j.tma.2025.02.002","DOIUrl":"10.1016/j.tma.2025.02.002","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the gradual loss of dopaminergic neurons in the substantia nigra, resulting in both motor and non-motor symptoms. A defining feature of PD pathology is the presence of Lewy bodies, which are intracellular inclusions primarily composed of aggregated alpha-synuclein (α-syn) proteins. The abnormal buildup of α-syn, referred to as α-synucleopathy, is a key aspect of PD and other neurodegenerative conditions. Recent research indicates that bacterial amyloids, such as curli proteins produced by <em>Escherichia coli</em>, may influence α-syn aggregation, potentially playing a role in PD development. These discoveries provide a new perspective on the involvement of microbial factors in neurodegenerative diseases, suggesting that curli proteins can cross-seed with α-syn and enhance its aggregation. Understanding these interactions opens up new therapeutic possibilities, including methods to inhibit curli production, prevent curli-α-syn interactions, or target the resulting pathological aggregates. Such therapeutic strategies could offer promising new ways to slow or stop the progression of PD and improve outcomes for patients.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 41-48"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2025.11.001
Brea J. Ford , Anisha Banerjee , Sarah Ding , Anna A. Caton , Ashley Grothaus , Sara N. Burke , Abbi R. Hernandez
Mitochondrial dysfunction is a hallmark of aging, affecting multiple systems and tissues, contributing to impairments in function. The resultant decreases in energy availability, along with increased oxidative stress, may be attenuated through diet. Fasting paradigms (including time restricted feeding (TRF)) and ketogenic diets (keto) both influence mitochondrial function, potentially mitigating these effects. However, the duration and modality of dietary intervention required for ameliorating age-related mitochondrial impairments remain unknown. Therefore, this study investigated the effects of a chronically (8–24 months; cTRFc) and acutely (22–24 months; aTRFc) administered TRF diet with standard macronutrients, as well as a chronically (8–24 months) administered TRF with ketogenic macronutrients (cTRFk), on mitochondrial activity and gene expression in aged male rats across tissues (brain, liver, muscle). Despite some synergy across the chronic diet groups, keto and TRF duration influenced mitochondrial function in a tissue- and diet-specific manner. Mitochondrial complex II activity was higher in cTRFk rats within the liver. Mitochondrial complex IV activity was lower in muscle and hippocampal tissue in both chronic TRF-fed groups. Relatedly, expression of the complex IV-related gene Cox2 increased within the CA3 subregion of the hippocampus of cTRFk. In this same region, expression of the mitochondrial biogenesis related gene Pgc1a was increased in cTRFc diet rats only. Within the liver, Cox5b expression increased in both groups of chronic TRF rats. Together, these findings highlight complex, tissue-specific responses to long-term dietary interventions, emphasizing the need for further research to develop targeted nutritional strategies for enhancing mitochondrial function and metabolic health in aging populations.
{"title":"Dietary duration and composition differentially influence mitochondrial activity and gene expression in a tissue-specific manner in aged rats","authors":"Brea J. Ford , Anisha Banerjee , Sarah Ding , Anna A. Caton , Ashley Grothaus , Sara N. Burke , Abbi R. Hernandez","doi":"10.1016/j.tma.2025.11.001","DOIUrl":"10.1016/j.tma.2025.11.001","url":null,"abstract":"<div><div>Mitochondrial dysfunction is a hallmark of aging, affecting multiple systems and tissues, contributing to impairments in function. The resultant decreases in energy availability, along with increased oxidative stress, may be attenuated through diet. Fasting paradigms (including time restricted feeding (TRF)) and ketogenic diets (keto) both influence mitochondrial function, potentially mitigating these effects. However, the duration and modality of dietary intervention required for ameliorating age-related mitochondrial impairments remain unknown. Therefore, this study investigated the effects of a chronically (8–24 months; cTRFc) and acutely (22–24 months; aTRFc) administered TRF diet with standard macronutrients, as well as a chronically (8–24 months) administered TRF with ketogenic macronutrients (cTRFk), on mitochondrial activity and gene expression in aged male rats across tissues (brain, liver, muscle). Despite some synergy across the chronic diet groups, keto and TRF duration influenced mitochondrial function in a tissue- and diet-specific manner. Mitochondrial complex II activity was higher in cTRFk rats within the liver. Mitochondrial complex IV activity was lower in muscle and hippocampal tissue in both chronic TRF-fed groups. Relatedly, expression of the complex IV-related gene <em>Cox2</em> increased within the CA3 subregion of the hippocampus of cTRFk. In this same region, expression of the mitochondrial biogenesis related gene <em>Pgc1a</em> was increased in cTRFc diet rats only. Within the liver, <em>Cox5b</em> expression increased in both groups of chronic TRF rats. Together, these findings highlight complex, tissue-specific responses to long-term dietary interventions, emphasizing the need for further research to develop targeted nutritional strategies for enhancing mitochondrial function and metabolic health in aging populations.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 100-107"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145614634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2025.08.004
Fenton Lam , Renfen Chen , Daniel Kam Yin Chan
Vascular dementia (VaD) is the second most common form of dementia after Alzheimer's disease and results from cerebrovascular pathology leading to brain tissue damage. This mini-review synthesizes current evidence on the interplay between diet, gut microbiota, and inflammation in the pathogenesis of VaD. Despite its significant global prevalence, there remains no effective pharmacological treatment for VaD, highlighting the need for preventative strategies. Emerging research suggests that the gut microbiome, diet, and systemic inflammation may collectively play a crucial role in the development and progression of VaD. The gut microbiome, a key regulator of immune function, has been implicated in neuroinflammation and cognitive decline, with microbial imbalances associated with elevated systemic inflammation and breakdown of blood brain barrier integrity. Furthermore, dietary patterns influence both gut microbiota composition and inflammatory status, with pro-inflammatory diets correlating with higher dementia risk and anti-inflammatory diets showing potential neuroprotective effects. A better understanding of these relationships could inform novel prevention and treatment strategies, including microbiome-targeted therapies such as probiotics and faecal microbiota transplantation.
{"title":"The role of diet, gut microbiome, and inflammation in vascular dementia: a mini review","authors":"Fenton Lam , Renfen Chen , Daniel Kam Yin Chan","doi":"10.1016/j.tma.2025.08.004","DOIUrl":"10.1016/j.tma.2025.08.004","url":null,"abstract":"<div><div>Vascular dementia (VaD) is the second most common form of dementia after Alzheimer's disease and results from cerebrovascular pathology leading to brain tissue damage. This mini-review synthesizes current evidence on the interplay between diet, gut microbiota, and inflammation in the pathogenesis of VaD. Despite its significant global prevalence, there remains no effective pharmacological treatment for VaD, highlighting the need for preventative strategies. Emerging research suggests that the gut microbiome, diet, and systemic inflammation may collectively play a crucial role in the development and progression of VaD. The gut microbiome, a key regulator of immune function, has been implicated in neuroinflammation and cognitive decline, with microbial imbalances associated with elevated systemic inflammation and breakdown of blood brain barrier integrity. Furthermore, dietary patterns influence both gut microbiota composition and inflammatory status, with pro-inflammatory diets correlating with higher dementia risk and anti-inflammatory diets showing potential neuroprotective effects. A better understanding of these relationships could inform novel prevention and treatment strategies, including microbiome-targeted therapies such as probiotics and faecal microbiota transplantation.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 74-79"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145157420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2024.12.003
Zhi-Xia Li , Jing-Dong J. Han
Aging is intricately linked to cognitive decline and neurodegenerative diseases, with neural stem cells (NSCs) playing a crucial role in brain function maintenance and repair. We examine the age-related metabolic shifts in NSCs, such as alterations in mitochondrial dynamics and protein expression, and how these changes affect NSCs' function of neurogenesis. We discuss the functional decline in NSCs’ proliferation and self-renewal capacity, mainly in the hippocampus, and their implications for cognitive function and emotional regulation. We also highlight the potential of understanding these cellular changes within NSCs to develop novel therapeutic strategies for neurodegenerative diseases and brain injuries, emphasizing the importance of harnessing NSC therapy in aging-related conditions.
{"title":"Neural stem cells in aging","authors":"Zhi-Xia Li , Jing-Dong J. Han","doi":"10.1016/j.tma.2024.12.003","DOIUrl":"10.1016/j.tma.2024.12.003","url":null,"abstract":"<div><div>Aging is intricately linked to cognitive decline and neurodegenerative diseases, with neural stem cells (NSCs) playing a crucial role in brain function maintenance and repair. We examine the age-related metabolic shifts in NSCs, such as alterations in mitochondrial dynamics and protein expression, and how these changes affect NSCs' function of neurogenesis. We discuss the functional decline in NSCs’ proliferation and self-renewal capacity, mainly in the hippocampus, and their implications for cognitive function and emotional regulation. We also highlight the potential of understanding these cellular changes within NSCs to develop novel therapeutic strategies for neurodegenerative diseases and brain injuries, emphasizing the importance of harnessing NSC therapy in aging-related conditions.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 9-14"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143139476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aging is the strongest risk factor for neurodegenerative diseases and has been implicated in important changes in the brain. Rodents, such as mice, have been used to understand age-related changes in brain function, and aging has been studied using senescence-accelerated mouse (SAM) strains. Accumulating evidence indicates that SAM-prone (SAMP)8 and SAMP10 strains have learning disabilities. However, in previous studies, these strains were not subjected to a series of behavioural tests. In behavioural experiments, it is necessary to conduct a behavioural test battery to consider various aspects, including sources of variability and experimental interference.
Method
This study aimed to comprehensively characterize behavioural abnormalities in SAMP8 and SAMP10 mice using a standardized battery of behavioural tests. We conducted a series of behavioural tests (neuromuscular strength, elevated plus maze, light-dark transition, open field, Y-maze, and passive avoidance tests) to investigate behaviour in SAMP8 and SAMP10 strains. We used 12-month-old male mice in this study.
Results
SAMP8 and SAMP10 mice exhibited abnormal behaviour in the present behavioural tests. Body weight, body temperature, muscle strength, and motor learning differed between SAMP8 or SAMP10 and SAMR1 mice. These differences may underlie variations in anxiety-like behaviours and locomotor activity.
Conclusion
Together, these findings highlight the utility of SAMP8 and SAMP10 mice as models for studying age-related functional decline in the brain.
{"title":"Comprehensive behavioural study of senescence-accelerated mouse prone 8 and senescence-accelerated mouse prone 10","authors":"Hiroshi Ueno , Yu Takahashi , Shinji Murakami , Kenta Wani , Tetsuji Miyazaki , Yosuke Matsumoto , Motoi Okamoto , Takeshi Ishihara","doi":"10.1016/j.tma.2025.08.003","DOIUrl":"10.1016/j.tma.2025.08.003","url":null,"abstract":"<div><h3>Background</h3><div>Aging is the strongest risk factor for neurodegenerative diseases and has been implicated in important changes in the brain. Rodents, such as mice, have been used to understand age-related changes in brain function, and aging has been studied using senescence-accelerated mouse (SAM) strains. Accumulating evidence indicates that SAM-prone (SAMP)8 and SAMP10 strains have learning disabilities. However, in previous studies, these strains were not subjected to a series of behavioural tests. In behavioural experiments, it is necessary to conduct a behavioural test battery to consider various aspects, including sources of variability and experimental interference.</div></div><div><h3>Method</h3><div>This study aimed to comprehensively characterize behavioural abnormalities in SAMP8 and SAMP10 mice using a standardized battery of behavioural tests. We conducted a series of behavioural tests (neuromuscular strength, elevated plus maze, light-dark transition, open field, Y-maze, and passive avoidance tests) to investigate behaviour in SAMP8 and SAMP10 strains. We used 12-month-old male mice in this study.</div></div><div><h3>Results</h3><div>SAMP8 and SAMP10 mice exhibited abnormal behaviour in the present behavioural tests. Body weight, body temperature, muscle strength, and motor learning differed between SAMP8 or SAMP10 and SAMR1 mice. These differences may underlie variations in anxiety-like behaviours and locomotor activity.</div></div><div><h3>Conclusion</h3><div>Together, these findings highlight the utility of SAMP8 and SAMP10 mice as models for studying age-related functional decline in the brain.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 55-65"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144851877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.tma.2025.02.001
Juan I. Bravo , Lucia Zhang , Bérénice A. Benayoun
LINE-1 (L1) and Alu are two families of transposable elements (TEs) occupying ∼17 % and ∼11 % of the human genome, respectively. Though only a small fraction of L1 copies is able to produce the machinery to mobilize autonomously, Alu and degenerate L1s can hijack their functional machinery and mobilize in trans. The expression and subsequent mobilization of L1 and Alu can exert pathological effects on their hosts. These features have made them promising focus subjects in studies of aging where they can become active. However, mechanisms regulating TE activity are incompletely characterized, especially in diverse human populations. To address these gaps, we leveraged genomic data from the 1000 Genomes Project to carry out a trans-ethnic GWAS of L1/Alu insertion singletons. These are rare, recently acquired insertions observed in only one person and which we used as proxies for variation in L1/Alu insertion numbers. Our approach identified SNVs in genomic regions containing genes with potential and known TE regulatory properties, and it enriched for SNVs in regions containing known regulators of L1 expression. Moreover, we identified reference TE copies and structural variants that associated with L1/Alu singletons, suggesting their potential contribution to TE insertion number variation. Finally, a transcriptional analysis of lymphoblastoid cells highlighted potential cell cycle alterations in a subset of samples harboring L1/Alu singletons. Collectively, our results suggest that known TE regulatory mechanisms may be active in diverse human populations, expand the list of loci implicated in TE insertion number variability, and reinforce links between TEs and disease.
{"title":"Multi-ancestry GWAS reveals loci linked to human variation in LINE-1- and Alu-insertion numbers","authors":"Juan I. Bravo , Lucia Zhang , Bérénice A. Benayoun","doi":"10.1016/j.tma.2025.02.001","DOIUrl":"10.1016/j.tma.2025.02.001","url":null,"abstract":"<div><div>LINE-1 (L1) and Alu are two families of transposable elements (TEs) occupying ∼17 % and ∼11 % of the human genome, respectively. Though only a small fraction of L1 copies is able to produce the machinery to mobilize autonomously, Alu and degenerate L1s can hijack their functional machinery and mobilize <em>in trans</em>. The expression and subsequent mobilization of L1 and Alu can exert pathological effects on their hosts. These features have made them promising focus subjects in studies of aging where they can become active. However, mechanisms regulating TE activity are incompletely characterized, especially in diverse human populations. To address these gaps, we leveraged genomic data from the 1000 Genomes Project to carry out a trans-ethnic GWAS of L1/Alu insertion singletons. These are rare, recently acquired insertions observed in only one person and which we used as proxies for variation in L1/Alu insertion numbers. Our approach identified SNVs in genomic regions containing genes with potential and known TE regulatory properties, and it enriched for SNVs in regions containing known regulators of L1 expression. Moreover, we identified reference TE copies and structural variants that associated with L1/Alu singletons, suggesting their potential contribution to TE insertion number variation. Finally, a transcriptional analysis of lymphoblastoid cells highlighted potential cell cycle alterations in a subset of samples harboring L1/Alu singletons. Collectively, our results suggest that known TE regulatory mechanisms may be active in diverse human populations, expand the list of loci implicated in TE insertion number variability, and reinforce links between TEs and disease.</div></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"9 ","pages":"Pages 25-40"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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