GeroScience最新文献

{"title":"Innovative approaches in the treatment-resistant depression: exploring different therapeutic pathways","authors":"Anna Łysik, Katarzyna Logoń, Aleksandra Szczygieł, Julia Wołoszczak, Martyna Wrześniewska, Jerzy Leszek","doi":"10.1007/s11357-025-01615-8","DOIUrl":"https://doi.org/10.1007/s11357-025-01615-8","url":null,"abstract":"<p>Treatment-resistant depression (TRD) remains a vital challenge in psychiatry, affecting a significant number of patients with major depressive disorder. Current pharmacological approaches often do not provide sufficient therapeutic results, prompting the need for innovative treatments. This review summarizes recent advances in TRD management, including non-pharmacological therapies such as transcranial magnetic stimulation, deep brain stimulation, electroconvulsive therapy, and vagus nerve stimulation, and describes their mechanisms of action. Novel pharmacotherapies, particularly glutamatergic modulators like ketamine and esketamine, have shown promising results with esketamine being available to eligible patients in Poland since 2023 within a drug program. Electroconvulsive therapy remains an effective treatment for TRD, usually with small side effects mainly including transient memory impairment, headache, or cardiovascular changes. Transcranial magnetic stimulation is a non-invasive procedure with proven efficacy; therefore several psychiatric organizations recommend it as a treatment option for major depressive disorder in their clinical guidelines. Deep brain stimulation is a relatively new treatment modality for TRD, with its primary risk being associated with the required neurosurgical procedure. Vagus nerve stimulation seems to be a promising adjunctive treatment for TRD, showing significant improvements in depressive symptoms, especially at higher electrical doses but with no side effects. While these treatments appear to have potential, personalized approaches are crucial for optimizing outcomes. Future research should focus on refining the techniques, improving safety profiles, and validating the long-term efficacy.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"7 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional ultrasound imaging reveals microvascular rarefaction, decreased cerebral blood flow, and impaired neurovascular coupling in a mouse model of paclitaxel-induced chemobrain","authors":"Siva Sai Chandragiri, Adam Nyul-Toth, Sharon Negri, Roland Patai, Rafal Gulej, Boglarka Csik, Santny Shanmugarama, Kiana Vali Kordestan, Mark Nagykaldi, Peter Mukli, Anna Ungvari, Andriy Yabluchanskiy, Zoltan Ungvari, Stefano Tarantini, Anna Csiszar","doi":"10.1007/s11357-025-01624-7","DOIUrl":"https://doi.org/10.1007/s11357-025-01624-7","url":null,"abstract":"<p>Chemotherapy-induced cognitive impairment (CICI), often referred to as “chemobrain,” significantly affects the quality of life in cancer survivors. Although traditionally attributed to neuronal toxicity, emerging evidence suggests a key role of cerebrovascular dysfunction in its pathogenesis. We hypothesized that paclitaxel (PTX, Taxol) treatment induces long-term cerebrovascular dysfunction, including microvascular rarefaction, impaired neurovascular coupling (NVC), and altered cerebral blood flow (CBF), which contribute to CICI. Using a clinically relevant PTX treatment regimen in non-tumor-bearing mice, we evaluated the long-term effects of PTX on cerebrovascular health. Ultrasound localization microscopy (ULM) and functional ultrasound imaging (fUS) were employed to assess microvascular density, CBF, and NVC. PTX treatment resulted in a significant reduction in microvascular density in the cerebral cortex and hippocampus, key regions involved in cognitive function. PTX significantly reduced blood velocity in the middle cerebral artery. Moreover, PTX impaired NVC responses, as evidenced by a diminished CBF increase in response to whisker stimulation, indicative of impaired reactive hyperemia. In conclusion, these findings demonstrate that PTX induces long-lasting cerebrovascular dysfunction, including microvascular rarefaction, impaired NVC, and altered CBF dynamics, which likely contribute to CICI. This study underscores the critical role of cerebrovascular health in cognitive function and highlights the potential of targeting cerebrovascular pathways as a therapeutic approach for mitigating chemotherapy-induced cognitive deficits.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"16 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic impact of a senescence gene signature in multiple myeloma","authors":"Andrea Lehoczki, Otilia Menyhart, Hajnalka Andrikovics, Monika Fekete, Csaba Kiss, Gabor Mikala, Zoltan Ungvari, Balázs Győrffy","doi":"10.1007/s11357-025-01622-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01622-9","url":null,"abstract":"<p>Multiple myeloma (MM), an incurable malignancy of plasma cells, is predominantly an age-related disease, with the majority of cases occurring in patients over the age of 60. Cellular senescence, a fundamental biological process underlying aging, has been increasingly recognized for its critical role in developing age-related malignancies. In this study, we aimed to investigate the prognostic significance of genes implicated in the molecular mechanisms of senescence within a large cohort of MM patients. Gene expression and clinical data from 1416 MM patients were obtained from four GEO datasets (GSE24080, GSE4204, GSE57317, and GSE9782) and integrated into a unified database. The raw data were processed using MAS5 normalization, scaling adjustments, and JetSet probe selection to ensure cross-platform comparability. A curated set of senescence-associated genes, the SenMayo gene signature, was employed for subsequent analyses. The final gene signature was computed as a weighted mean expression of 122 senescence-associated genes, with weights derived from univariate hazard ratios. Prognostic significance was evaluated using Cox regression, Kaplan–Meier survival analysis, and multivariate models incorporating clinical parameters such as gender, isotype, and molecular subtypes. False discovery rate (FDR) correction was applied to ensure the statistical robustness of findings. The weighted SenMayo gene signature strongly correlated with overall survival in MM patients (HR = 0.6, 95% CI = 0.47–0.76, <i>p</i> = 1.7e-05). The 75th percent probability of survival was reached at 36.1 months in the low-expression patient group, compared to 57 months in the high-expression group. Independent validation in datasets with sufficient patient numbers confirmed the prognostic value of the SenMayo signature (GSE4204: HR = 0.58, 95% CI = 0.39–0.88, <i>p</i> = 0.0089; GSE24080: HR = 0.61, 95% CI = 0.45–0.83, <i>p</i> = 0.0012; GSE57317: HR = 0.25, 95% CI = 0.08–0.77, <i>p</i> = 0.0095). Multivariate analyses further established the SenMayo signature as an independent prognostic factor, even when accounting for established clinical parameters such as sex and isotype. These findings underscore the robustness and independence of the SenMayo gene signature as a predictor of overall survival in multiple myeloma. This signature provides clinically valuable insights into the role of cellular senescence in disease progression.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"28 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143703049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: White matter lipid alterations during aging in the rhesus monkey brain","authors":"Christina Dimovasili, Ana T. Vitantonio, Bryce Conner, Kelli L. Vaughan, Julie A. Mattison, Douglas L. Rosene","doi":"10.1007/s11357-025-01620-x","DOIUrl":"https://doi.org/10.1007/s11357-025-01620-x","url":null,"abstract":"","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"24 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical adaptations in regional activity and backbone network following short-term postural training with visual feedback for older adults","authors":"Yi-Ching Chen, Yi-Ying Tsai, Wei-Min Huang, Chen-Guang Zhao, Ing-Shiou Hwang","doi":"10.1007/s11357-025-01614-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01614-9","url":null,"abstract":"<p>This study investigated cortical reorganization in older adults following short-term interactive balance training. Twenty participants aged 65–74 received training in stabilometer stance, visually aligning plate movement with a horizontal line on a monitor. Pre-test and post-test measured posture fluctuations and scalp EEG during stabilometer stance. Results showed a training-related decrease in root mean square (RMS) (<i>p</i> = 0.001) and an increase in mean frequency (<i>p</i> = 0.006) of posture fluctuations. Despite a decline in theta relative power in Fp1 (<i>p</i> = 0.027), stabilometer training led to a post-test increase in alpha relative power around electrodes of the ventral visual pathway (<i>p</i> = 0.002). Additionally, augmentations were noted in theta relative power in Tp8 (<i>p</i> = 0.033) and beta relative power in F7 (<i>p</i> = 0.039). Analysis of the minimum spanning tree (MST) of alpha inter-regional connectivity indicated a training-related decrease in leaf fraction (<i>p</i> = 0.011) and increase in average eccentricity (<i>p</i> = 0.041), respectively. Training-related changes in the RMS of posture fluctuation were positively correlated with changes in pooled alpha relative power in electrodes of the ventral visual pathway (<i>r</i> = 0.459, <i>p</i> = 0.042) and negatively correlated with changes in average eccentricity of the alpha MST network (<i>r</i> = − 0.487, <i>p</i> = 0.029). In conclusion, short-term interactive training enhances balance by reorganizing regional and alpha-band network activities, which supports improved visual attention and prevents early visual processing idling during initial postural learning.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"123 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis?","authors":"Anna Ungvari, Ádám Nyúl-Tóth, Roland Patai, Boglarka Csik, Rafal Gulej, Dorina Nagy, Santny Shanmugarama, Zoltán Benyó, Tamas Kiss, Zoltan Ungvari, Anna Csiszar","doi":"10.1007/s11357-025-01621-w","DOIUrl":"https://doi.org/10.1007/s11357-025-01621-w","url":null,"abstract":"<p>Vascular cognitive impairment (VCI) is a leading cause of age-related cognitive decline, driven by cerebrovascular dysfunction and cerebral small vessel disease (CSVD). Emerging evidence suggests that cerebromicrovascular endothelial senescence plays an important role in the pathogenesis of VCI by promoting cerebral blood flow dysregulation, neurovascular uncoupling, blood–brain barrier (BBB) disruption, and the development of cerebral microhemorrhages (CMHs). This review explores the concept of cerebromicrovascular senescence as a continuum of vascular aging, linking macrovascular atherosclerosis with microvascular dysfunction. It examines the mechanisms by which endothelial senescence drives neurovascular pathology and highlights the impact of cardiovascular risk factors in accelerating these processes. We examine preclinical and clinical studies that provide compelling evidence that atherosclerosis-induced microvascular senescence exacerbates cognitive impairment. In particular, findings suggest that targeting senescent endothelial cells through senolytic therapy can restore cerebrovascular function and improve cognitive outcomes in experimental models of atherosclerosis. Given the growing recognition of microvascular senescence as a therapeutic target, further research is warranted to explore novel interventions such as senolytics, anti-inflammatory agents, and metabolic modulators. The development of circulating biomarkers of vascular senescence (e.g., senescence-associated secretory phenotype [SASP] components and endothelial-derived extracellular vesicles) could enable early detection and risk stratification in individuals at high risk for VCI. Additionally, lifestyle modifications, including the Mediterranean diet, hold promise for delaying endothelial senescence and mitigating cognitive decline. In conclusion, cerebromicrovascular senescence is a key mechanistic link between atherosclerosis and cognitive impairment. Addressing microvascular aging as a modifiable risk factor through targeted interventions offers a promising strategy for reducing the burden of VCI and preserving cognitive function in aging populations.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"92 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic alcohol consumption accelerates cardiovascular aging and decreases cardiovascular reserve capacity","authors":"Partha Mukhopadhyay, Burhan Yokus, Bruno Paes-Leme, Sándor Bátkai, Zoltán Ungvári, György Haskó, Pal Pacher","doi":"10.1007/s11357-025-01613-w","DOIUrl":"https://doi.org/10.1007/s11357-025-01613-w","url":null,"abstract":"<p>The pathology of cardiovascular aging is complex, involving mitochondrial dysfunction, oxidative and nitrative stress, oxidative DNA injury, impaired lipid metabolism, cell death, senescence, and chronic inflammation. These processes lead to remodeling and structural changes in the cardiovascular system, resulting in a progressive decline in cardiovascular reserve capacity and health, and an increased risk of diseases and mortality. Excessive alcohol consumption exacerbates these risks by promoting hypertension, stroke, arrhythmias, coronary artery disease, cardiomyopathy, and sudden cardiac death, yet the effects of chronic alcohol consumption on cardiovascular aging remain unclear. Herein, we explored the impact of a 6-month 5% Lieber-DeCarli alcohol diet in young (3 months old) and aging (24–26 months old) Fisher F344BNF1 rats. We assessed detailed hemodynamics, mitochondrial function, oxidative/nitrative stress, lipid metabolism, inflammation, cell death, senescence, and myocardial fibrosis using the pressure–volume system, isolated vascular rings, and various histological, biochemical, and molecular biology methods. Alcohol consumption in both young and aging rats impaired mitochondrial function, disrupted cholesterol and triglyceride metabolism, and increased oxidative/nitrative stress, inflammation, cell death, and senescence, leading to a decline in systolic contractile function. In aging rats, alcohol further exacerbated diastolic dysfunction and myocardial fibrosis. Alcohol also increased oxidative/nitrative stress, apoptosis, and senescence in the vasculature, contributing to endothelial dysfunction and increased total peripheral resistance. Additionally, alcohol exacerbated the aging-related ventriculo-arterial uncoupling and diminished cardiac efficiency, further reducing cardiovascular reserve capacity. In conclusion, chronic alcohol consumption promotes cardiovascular aging and further diminishes the already impaired cardiac and vascular reserve capacity associated with aging.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"34 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-related alterations of angiogenesis, inflammation and bone microarchitecture during fracture healing in mice","authors":"Maximilian M. Menger, Ruben Manuschewski, Sandra Hans, Benedikt J. Braun, Moses K. D. El Kayali, Sabrina Ehnert, Emmanuel Ampofo, Selina Wrublewsky, Michael D. Menger, Tina Histing, Matthias W. Laschke","doi":"10.1007/s11357-025-01584-y","DOIUrl":"https://doi.org/10.1007/s11357-025-01584-y","url":null,"abstract":"<p>The surgical treatment of geriatric patients represents a major challenge in traumatology. It is well known that aging affects fracture healing. However, the exact pathophysiology of age-related changes in angiogenesis, inflammation and bone remodeling remains still elusive. Therefore, we herein studied the differences of femoral fracture healing in young adult (3–4 months) and aged (16–18 months) CD-1 mice by using a stable closed femoral fracture model with intramedullary screw fixation. The callus tissue was analyzed by means of X-ray, micro-computed tomography (µCT), histology and immunohistochemistry. We found a deteriorated trabecular architecture and a reduced bone formation within the callus tissue of aged mice. Moreover, aged animals showed an increased number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts at an early healing time point, whereas the fraction of mature α-smooth muscle actin (SMA)-positive microvessels was significantly reduced. Furthermore, the numbers of macrophages and granulocytes were higher in the callus tissue of aged animals at the end of the healing process. Taken together, these results demonstrate a delayed femoral fracture healing in aged CD-1 mice. This is most likely caused by an early overshooting osteoclast response, a decelerated maturation of the callus microvasculature and a late increased recruitment of pro-inflammatory cells. Targeting these alterations may contribute to the development of novel treatment approaches for the stimulation of bone regeneration in geriatric patients.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"92 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of acipimox on skeletal muscle biochemistry, structure and function in older people with probable sarcopenia: an experimental medicine study","authors":"Claire McDonald, Craig Alderson, Matthew G. Birkbeck, Silvia Del Din, Gráinne S. Gorman, Kieren G. Hollingsworth, Cameron Kirk, Clare Massarella, Lynn Rochester, Helen A. L. Tuppen, Charlotte Warren, Avan A. Sayer, Miles D. Witham","doi":"10.1007/s11357-025-01606-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01606-9","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Skeletal muscle nicotinamide adenine dinucleotide (NAD) concentrations are low in people with sarcopenia. Increasing NAD concentrations may offer a novel therapy. This study tested if acipimox (a NAD precursor) improves skeletal muscle NAD concentration and function in people with probable sarcopenia. Participants aged 65 and over with low walk speed (&lt; 0.8 m/s) and low muscle strength (by 2019 European Working Group criteria) were recruited to this before and after, proof-of-concept study. Participants received acipimox 250 mg orally (twice or thrice daily according to creatinine clearance) + aspirin 75 mg daily (to prevent facial flushing) for 4 weeks. Muscle biopsy of the vastus lateralis, ³¹P magnetic resonance spectroscopy and a 7-digital mobility assessment were performed before starting acipimox and after 3 weeks of treatment. The primary outcome was change in skeletal muscle NAD concentration. Secondary outcomes included change in phosphocreatine recovery rate and measures of physical performance. Eleven participants (8 women), mean age 78.9 years (SD 4.3), were recruited. Mean walk speed at baseline was 0.69 m/s (SD 0.07). All completed baseline and follow-up visits. Median medication adherence was 95% (range 91–104%). There was no statistically significant difference in the primary outcome of change in NAD concentrations in skeletal muscle between baseline and follow-up [median difference: − 0.003 umol/g (IQR − 0.058 to 0.210); <i>P</i> = 0.26] or secondary outcomes. Nineteen none-serious adverse events were reported. Although the study protocol was feasible and well tolerated, acipimox did not improve skeletal muscle NAD concentration, biochemical markers or physical function in people with probable sarcopenia. ClinicalTrials.gov Identifier: ISRCTN (ISRCTN87404878).</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"33 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An incidental finding during a brain plasticity study: substantial telomere length shortening after COVID-19 lockdown in the older population","authors":"Kirsten Jahn, Shambhabi Chatterjee, Christopher Sinke, Jonas Janik Ralf Koberschinski, Kristin Jünemann, Clara Eline James, Florian Worschech, Damien Marie, Eckart Altenmüller, Christian Bär, Tillmann Horst Christoph Krüger","doi":"10.1007/s11357-025-01602-z","DOIUrl":"https://doi.org/10.1007/s11357-025-01602-z","url":null,"abstract":"<p>The detrimental effects of lockdowns have already been proven by numerous studies, mainly using psychometric measurements. Since telomere shortening is a driver of aging and aging-associated disorders, including cognitive decline, the telomere length in the older population has been investigated in the current study. Measurements were taken over a 6-month period just before and during the 6 months that included the first lockdown. The cohort of 55 persons aged 64 to 70 years was investigated in the context of a study focusing on neuroplasticity. Participants were recruited in Germany and Switzerland and characterized by psychometric measurements concerning neurocognition and neuroplasticity. Telomere lengths were measured by real-time PCR-based LTL measurement. We found an impressive and significant decline in telomere lengths in the period that included the lockdown (2.33 (± 0.1) at T1 vs. 1.35 (± 0.1) at T2), whereas it was stable in the phase before the lockdown in the same individuals (T0 was 2.25 (± 0.1 S.E.M.) vs. T1, 2.33 (± 0.1)). Correlation of the sudden decrease revealed no linkage to health issues or general physical activity but was in trend related to a decline in the WHOQOL-BREF Social Score referring to the social interaction of the study participants. Our data support, at a biological level, the results of clinical and psychosocial studies showing the detrimental effects of lockdowns.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"42 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}