Translational Medicine of Aging最新文献

{"title":"Subjective cognitive decline and cerebral-cognitive reserve in late age","authors":"Alena Sidenkova ,&nbsp;Vittorio Calabrese ,&nbsp;Mario Tomasello ,&nbsp;Tilman Fritsch","doi":"10.1016/j.tma.2023.11.001","DOIUrl":"https://doi.org/10.1016/j.tma.2023.11.001","url":null,"abstract":"<div><p>Determining the boundaries of the norm and pathology of mental aging is an urgent scientific task. We have formulated a hypothesis about the presence of a transitional period within the cognitive continuum, which represents a borderline between normality and cognitive disorder; such a transitional state is subjective cognitive decline. The outcome of this period depends on the interaction between disease factors and protective factors, one of which is cognitive reserve.</p></div><div><h3>The purpose</h3><p>of this review is to systematize the current data in the field of research on subjective cognitive decline and protective factors that prevent its transformation into cognitive disorder.</p></div><div><h3>Materials and methods of research</h3><p>A systematic review of scientific studies was conducted. The search was conducted using PubMed using the keywords: “subjective cognitive decline”, “subjective cognitive impairment”, “cerebral reserve”, “cognitive reserve”, “Alzheimer's disease”. The review includes an analysis of 126 full-text literature sources. The significance of cerebral-cognitive reserve at various stages of AD and the diagnostic boundaries of the concepts “Preclinical conditions of AD” and “Subjective cognitive decline” are analyzed.</p></div><div><h3>Conclusions</h3><p>The analysis of scientific literature has shown the absence of clear terminological and diagnostic boundaries regarding the definition of the preclinical stage of the disease and compensatory mechanisms that deter the breakthrough of the disease into clinical level. At each stage of Alzheimer's disease there is an interaction between destructive and protective processes. The reserve plays a protective role; it delays the onset of clinical manifestations of Alzheimer's disease. The subjective cognitive decline is a transitional stage from a phenomenological cognitive norm to a clinically manifested pathology. As Alzheimer's disease progresses, there is a transition from the protective role of the reserve to its compensatory function. The defense mechanisms underlying the reserve concept are partially controllable, which makes it possible to build strategies for correcting cellular homeostasis, brain functions, behavioral and cognitive patterns.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"7 ","pages":"Pages 137-147"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468501123000172/pdfft?md5=c27a9de3cde22f65264aa8599e5456c9&pid=1-s2.0-S2468501123000172-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138769948","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}

{"title":"Effects of cocoa on altered metabolite levels in purine metabolism pathways and urea cycle in Alzheimer's disease in C. elegans","authors":"Mihiri Munasinghe ,&nbsp;Roya Afshari ,&nbsp;Deniz Heydarian ,&nbsp;Abdullah Almotayri ,&nbsp;Daniel A. Dias ,&nbsp;Jency Thomas ,&nbsp;Markandeya Jois","doi":"10.1016/j.tma.2022.10.001","DOIUrl":"10.1016/j.tma.2022.10.001","url":null,"abstract":"<div><p>Dietary interventions have gained much attention as alternative therapies in aging-associated diseases. Epidemiological studies suggest that polyphenols (PPs) play an important role in this regard. Cocoa is rich in PPs, greater in amount than in teas and red wine. This study aimed to characterize the age-associated and amyloid-β (Aβ)-induced changes in metabolism in <em>C. elegans</em> and the effects of cocoa supplementation. An untargeted Gas Chromatography-Mass Spectrometry (GC-MS) approach was used to determine the changes in endogenous metabolite levels in wild-type and a transgenic <em>C. elegans</em> strain expressing pan-neuronal Aβ (GRU102). Aging appeared to alter some amino acid levels in <em>C. elegans</em>. Cocoa supplementation reduced leucine and tyrosine levels in old age (day 12). GRU102 showed higher proline and asparagine relative to control worms at a young age (day 4) which may have a connection with cognitive deficits in Alzheimer's disease (AD). Cocoa reduced the elevated levels of these two amino acids to the levels in the control worms. The purine derivative, hypoxanthine was higher in GRU102 relative to the control worms at their middle age (day 8) where the elevated are known to contribute to memory deficits in AD. Cocoa supplementation reduced the elevated hypoxanthine to normal levels. Aβ expression showed alterations in the urea cycle in worms in their middle age as indicated by increased ornithine.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"6 ","pages":"Pages 14-24"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468501122000013/pdfft?md5=0d05274298622269d62419ac34e6754a&pid=1-s2.0-S2468501122000013-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47729256","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}

{"title":"Tuning up an aged clock: Circadian clock regulation in metabolism and aging","authors":"Shogo Sato ,&nbsp;Guiomar Solanas ,&nbsp;Paolo Sassone-Corsi ,&nbsp;Salvador Aznar Benitah","doi":"10.1016/j.tma.2021.11.003","DOIUrl":"10.1016/j.tma.2021.11.003","url":null,"abstract":"<div><p>Circadian rhythms provide temporal variation of a broad range of behavioral and physiological functions, which is precisely controlled by the internal molecular gear, the circadian clock. However, circadian clock functions decline concomitantly with aging-dependent functional deterioration, such as metabolic dysfunction. Metabolic deterioration is widely accepted as one of the hallmarks of aging and leads to various types of aging-associated diseases, such as type 2 diabetes, cardiovascular disease, cancer, and Alzheimer's disease. Importantly, recent transcriptomic, epigenomic, proteomic, and metabolomic data indicates that the circadian clock governs daily fluctuation of metabolic activity and in turn is functionally reliant on metabolic and epigenetic modifications. This suggests that the activation of the circadian clock defends organisms from metabolic aging, eventually resulting in systemic healthy aging. This notion is strongly supported by mounting evidence indicating that dietary interventions robustly affect the circadian clock machinery and subsequent clock-controlled metabolic pathways. In the 21st century, the expansion of an aged population is one of the most important health problem worldwide, making a strategy to promote healthy aging critical. In this review, we summarize the latest evidence regarding an intertwined link between aging and the circadian clock, and propose potential anti-aging therapies centered on the circadian clock.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"6 ","pages":"Pages 1-13"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468501121000080/pdfft?md5=3bfe948c36ac611c5eedcb551449491a&pid=1-s2.0-S2468501121000080-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46134180","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}

{"title":"High calorie diet background alters the expression of sirtuins in the testes of mice under caloric restriction","authors":"Martin Maldonado ,&nbsp;Jianying Chen ,&nbsp;Huiqin Duan,&nbsp;Tianhua Huang,&nbsp;Gu Jiang,&nbsp;Ying Zhong","doi":"10.1016/j.tma.2021.02.001","DOIUrl":"10.1016/j.tma.2021.02.001","url":null,"abstract":"<div><p>Caloric restriction (CR) is considered one of the most efficient interventions that extend lifespan and healthspan by delaying the onset of many age-related diseases in a variety of organisms. CR appears to activate sirtuins, which in turn modulate a wide range of cellular activities related to pathophysiological conditions such as stress and inflammation, DNA repair, apoptosis, and the processes of aging.</p><p>In this work we aimed to determine whether CR can counteract the detrimental effects of a high-calorie diet (HCD) on the mRNA and protein levels of sirtuins in testes of a murine experimental model.</p><p>We report in here that short-term CR increased the mRNA and protein expression of all sirtuins in the animals previously feed standard food. However, short-term CR failed to activate sirtuins in the animals previously fed an HCD for a period of 4 months. Moreover, histologic analysis of adipocyte/lipid infiltration by oil red O assay, in the mice testis, showed that the highest lipid content was found in the animals with an HCD background, exposed to CR.</p><p>Mechanistic actions, as well as substrates that modify sirtuins transcriptional and translational expression in the mice male reproductive system, are still not well understood. We believe that deeper insights into how the potential selective modulation of SIRT family members and sirtuins activators affect the different organs, individually and as a whole system will eventually led to the development of preventative and therapeutic strategies to promote health and longevity.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 10-16"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2021.02.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175813","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}

{"title":"Targeting senescent cell clearance: An approach to delay aging and age-associated disorders","authors":"Zhengqi Qiu,&nbsp;Jiali Jia,&nbsp;Haoman Zou,&nbsp;Ying Ao,&nbsp;Baohua Liu,&nbsp;Zimei Wang","doi":"10.1016/j.tma.2020.12.001","DOIUrl":"10.1016/j.tma.2020.12.001","url":null,"abstract":"<div><p>Cellular senescence is the occurrence of irreversible cell cycle arrest resulting from accumulated DNA damage and the loss of proteostasis over time. Senescent cells contribute to age-related diseases and aging itself. Therefore, the targeted elimination of senescent cells may be beneficial for long-term human health in general. In this review, we summarize three key areas of recent research into the clearance of senescent cells, including senolysis via senolytic drugs, immune-based senescent cell clearance, and neutralization of the senescence-associated secretory phenotype (SASP). Therapeutic strategies for the targeted clearance of senescent cells are being developed at a rapid pace, with some already undergoing clinical trials in humans. In the future, advances in the targeted clearance of senescent cells will undoubtedly yield further beneficial ways to improve human health during aging and increase human longevity.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 1-9"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2020.12.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175796","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}

{"title":"A single oral supplementation of nicotinamide within the daily tolerable upper level increases blood NAD+ levels in healthy subjects","authors":"Takashi K. Ito ,&nbsp;Tomohito Sato ,&nbsp;Yusuke Takanashi ,&nbsp;Zinat Tamannaa ,&nbsp;Takuya Kitamoto ,&nbsp;Keiichi Odagiri ,&nbsp;Mitsutoshi Setou","doi":"10.1016/j.tma.2021.09.001","DOIUrl":"10.1016/j.tma.2021.09.001","url":null,"abstract":"<div><p>A decrease in nicotinamide adenine dinucleotide (NAD⁺) levels is a hallmark of aging in multiple species, including humans. Our previous clinical trial showed that supplementation of 200 mg nicotinamide, a form of vitamin B3, increased blood NAD⁺ levels. Here we report a clinical trial to assess the efficacy of a lower and a higher dose nicotinamide on increasing NAD⁺ levels. Blood NAD⁺ levels were evaluated before and after treatment of 100 mg nicotinamide, 500 mg nicotinamide, or water only. The three treatment arms were tested in the same cohort of 5 healthy adults. Oral supplementation of 500 mg nicotinamide led to a significant increase in blood NAD⁺ after 12 h and showed a trend of increase after 48 h (<em>P</em> = 0.056), whereas 100 mg nicotinamide or water intake only did not change the NAD⁺ levels in the same subjects. Blood lipidome analysis showed that the levels of 277 lipid species significantly changed after 12 h among 1463 species detected, while no changes were detected at 0 h among the 3 groups. These lipid changes largely reflected the difference between the nicotinamide supplemented groups and the water control group. Together with our previous results, this study shows that oral supplementation of nicotinamide within the daily tolerable upper level is an effective way to transiently increase NAD⁺ levels and affect the composition of blood lipids.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 43-51"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468501121000055/pdfft?md5=1c52e048d43c9ea3ce2de640c940d754&pid=1-s2.0-S2468501121000055-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175843","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}

{"title":"Heart failure risk remote monitoring program in the very elderly patients with COVID-19 disease","authors":"Abrar-Ahmad Zulfiqar,&nbsp;Emmanuel Andres,&nbsp;Mohamed Hajjam,&nbsp;Delwendé Noaga Damien Massimbo,&nbsp;Amir Hajjam","doi":"10.1016/j.tma.2021.11.004","DOIUrl":"10.1016/j.tma.2021.11.004","url":null,"abstract":"","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 52-53"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8598265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39652978","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}

{"title":"Transcription errors in aging and disease","authors":"M.E. Anagnostou ,&nbsp;C. Chung ,&nbsp;E. McGann ,&nbsp;B.M. Verheijen ,&nbsp;Y. Kou ,&nbsp;L. Chen ,&nbsp;M. Vermulst","doi":"10.1016/j.tma.2021.05.002","DOIUrl":"10.1016/j.tma.2021.05.002","url":null,"abstract":"<div><p>Accurate transcription is required for the faithful expression of genetic information. However, little is known about the fidelity of RNA synthesis or the biological consequences of transcription errors in living cells. Here, we review recent developments in massively parallel sequencing technology that allow the fidelity of transcription to be measured with unprecedented accuracy and summarize new observations that provide insight into the role of transcription errors in aging and disease. Taken together, these developments have the potential to change our understanding of mutagenesis itself, and significantly enhance our understanding of the origins of human disease.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 31-38"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2021.05.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42649067","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}

{"title":"A chronic low dosage of taurine induces muscle weakness in castrated-aged mice","authors":"Noelia G. Barragán-Ceballos ,&nbsp;Juan C. Iglesias-Santos ,&nbsp;Daniel Perea-Ruiz ,&nbsp;Ana M. Guzman-Ambriz ,&nbsp;Andrómeda Liñan-Rico ,&nbsp;Rocío Zatarain-Palacios ,&nbsp;Adolfo Virgen-Ortiz ,&nbsp;Luis A. Castro-Sanchez ,&nbsp;Adan Dagnino-Acosta","doi":"10.1016/j.tma.2021.11.002","DOIUrl":"10.1016/j.tma.2021.11.002","url":null,"abstract":"<div><p>Taurine is an abundant metabolite associated with regulation of cell volume. Several signaling pathways are stimulated at a micromolar concentrations of taurine. However, most of the experimental studies employ this compound at a very high concentration (tens of millimolar). In this study, the role of a chronic treatment with a micromolar dosage of taurine in the physical performance of skeletal muscle of castrated-aged mice was characterized.</p><p>Taurine was administered in drinking water (800 μM) to 9-months-old castrated (or sham) mice at approximately 20 mg/kg per day for 12 weeks. The weight of the mice, grip strength, food and water intake were monitored. Soleus or EDL muscles were dissected for determinations of force and fatigue.</p><p>Castrated mice show a slow increase in body mass and a sustained reduction of grip strength. The taurine treatment delays the weigh recovery and generates a decrease in force of castrated and sham mice. No effect of taurine was observed in young mice. The food intake was significantly reduced in castrated mice treated with taurine (with no effect in water intake). The raw force generation or muscle mass in EDL and soleus muscle were similar in treated mice in comparison with control groups. Interestingly, the taurine treatment generated an increased fatigability in both EDL and soleus muscle.</p><p>We suggest that a submillimolar concentration of taurine, chronically administered during aging, produce negative effect in physical performance. Caution should be taken when this compound is routinely consumed by old adults.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 54-61"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468501121000079/pdfft?md5=e18dce177a633e51a57ecfe87ac5233e&pid=1-s2.0-S2468501121000079-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41628024","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}

{"title":"Validation of a new frailty scale in primary care: The simplified Zulfiqar frailty scale","authors":"Abrar-Ahmad ZULFIQAR M.D, MSc","doi":"10.1016/j.tma.2021.08.001","DOIUrl":"10.1016/j.tma.2021.08.001","url":null,"abstract":"<div><h3>Purpose</h3><p>Evaluate the ability of the “simplified Zulfiqar frailty scale” (sZFS) tool to detect frailty as defined by Fried's criteria among a group of patients aged 65 and older.</p></div><div><h3><strong>Methods</strong></h3><p>Prospective study conducted in Champagne-Ardennes (France) for 12 months on patients aged 65 and over and considered autonomous in terms of the ADL scale. To be eligible, the patients could not reside in a nursing home and needed an ADL score of 4 or higher.</p></div><div><h3><strong>Results</strong></h3><p>With this tool, the threshold for identifying frailty was≥1 out of 5 criteria. It was quick (average completion time of 110 s) with a sensitivity score of 91.1% and a negative predictive value of 97.1%.</p></div><div><h3><strong>Conclusion</strong></h3><p>The “simplified Zulfiqar frailty scale” tool measures frailty just as effectively as Fried's criteria, with sensitivity and negative predictive values no lower than the latter.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"5 ","pages":"Pages 39-42"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2021.08.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175833","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}