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436
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ShareScore release 0.9.0
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436 results for “Longevity”
Activated SKN-1 alters the longevity trajectory of long-lived C. elegans mutants
GEO Series GSE270810. Caenorhabditis elegans. 12 samples. Type: Expression profiling by high throughput sequencing.
The CRTC-1 transcriptional domain is required for COMPASS complex mediated longevity in C. elegans
GEO Series GSE239572. Caenorhabditis elegans. 16 samples. Type: Expression profiling by high throughput sequencing.
HSF-1 promotes longevity through ubiquilin-1 dependent mitochondrial remodelling
GEO Series GSE241558. Caenorhabditis elegans. 16 samples. Type: Expression profiling by high throughput sequencing.
Efficacy of longevity interventions in C. elegans is determined by early life activity of RNA splicing factors
GEO Series GSE292723. Caenorhabditis elegans. 12 samples. Type: Expression profiling by high throughput sequencing.
Fine-Tuning of PGC1α Expression Regulates Cardiac Function and Longevity
GEO Series GSE136787. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
Inhibition of sphingosine metabolism suppresses ferroptosis and rejuvenates aged hematopoietic stem cells to promote cognition and longevity [scRNA-seq]
GEO Series GSE287241. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
Unique sequence features define epigenetic longevity of inflammatory memory [scATAC-seq]
GEO Series GSE301537. Mus musculus. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Glial UDP-glycosyltransferase Ugt35b regulates longevity by maintaining lipid homeostasis in Drosophila
GEO Series GSE252680. Drosophila melanogaster. 6 samples. Type: Expression profiling by high throughput sequencing.
Association of rs3027178 polymorphism in the circadian clock gene PER1 with susceptibility to Alzheimer's disease and longevity in an Italian population
<p>Many physiological processes in the human body follow a 24-h circadian rhythm controlled by the circadian clock system. Light, sensed by retina, is the predominant "zeitgeber" able to synchronize the circadian rhythms to the light-dark cycles. Circadian rhythm dysfunction and sleep disorders have been associated with aging and neurodegenerative diseases including mild cognitive impairment (MCI) and Alzheimer's disease (AD). In the present study, we aimed at investigating the genetic variability of clock genes in AD patients compared to healthy controls from Italy. We also included a group of Italian centenarians, considered as super-controls in association studies given their extreme phenotype of successful aging. We analyzed the exon sequences of eighty-four genes related to circadian rhythms, and the most significant variants identified in this first discovery phase were further assessed in a larger independent cohort of AD patients by matrix assisted laser desorption/ionization-time of flight mass spectrometry. The results identified a significant association between the rs3027178 polymorphism in the PER1 circadian gene with AD, the G allele being protective for AD. Interestingly, rs3027178 showed similar genotypic frequencies among AD patients and centenarians. These results collectively underline the relevance of circadian dysfunction in the predisposition to AD and contribute to the discussion on the role of the relationship between the genetics of age-related diseases and of longevity.</p>
Data set related to the article: "Transfer of the longevity-associated variant of BPIFB4 gene rejuvenates immune system and vasculature by a reduction of CD38+ macrophages and NAD+ decline"
<p>As we age, our body experiences chronic, systemic inflammation contributing to the morbidity and mortality of the elderly. The senescent immune system has been described to have a causal role in driving systemic aging and therefore may represent a key therapeutic target to prevent pathological consequences associated with aging and extend a healthy lifespan. Previous studies from our group associated a polymorphic haplotype variant in the BPIFB4 gene (LAV-BPIFB4) with exceptional longevity. Transfer of the LAV-BPIFB4 in preclinical models halted the progression of cardiovascular diseases (CVDs) and frailty by counterbalancing chronic inflammation. In the present study, we aimed to delineate the action of systemic adeno-associated viral vector-mediated LAV-BPIFB4 gene transfer (AAV-LAV-BPIFB4) on the deleterious age-related changes of the immune system and thereby the senescence-associated events occurring in C57BL/6J mice aged 26 months. Our in vivo data showed that 26-months-old mice had a higher frequency of CD45+SA-beta Gal+ immune cells in peripheral blood than young (4-months-old) C57BL/6J mice. Notably, AAVLAV-BPIFB4 gene transfer in aged mice reduced the pool of peripheral immunosenescent cells that were shown to be enriched in the spleen. In addition, the proper tuning of the immune secretory phenotype (IL1βlow, IL6low, IL10high) associated with a significant reduction in SA-beta Gal-positive area of aorta from AAV-LAV treated mice. At the functional level, the reduction of senescenceassociated inflammation ensured sustained NAD+ levels in the plasma of AAV-LAV-BPIFB4 old mice by preventing the NADase CD38 increase in F4/80+ tissue-resident macrophages and Ly6Chigh pro-inflammatory monocytes of the spleen and bone marrow. Finally, to validate the clinical implication of our findings, we showed that Long-living-individuals (LLIs, >95 years), which delay CVDs onset, especially if LAV-carriers, were characterized by high NAD+ levels. In conclusion, the new senotherapeutic action of LAV-BPIFB4 may offer a valuable therapeutic tool to control aging and reduce the burden of its pathophysiological disorders, such as CVDs.</p>
Data set related to the article: "The longevity-associated BPIFB4 gene supports cardiac function and vascularization in ageing cardiomyopathy"
<p><strong>Aims</strong></p> <p>The ageing heart naturally incurs a progressive decline in function and perfusion that available treatments cannot halt. However,</p> <p>some exceptional individuals maintain good health until the very late stage of their life due to favourable gene–environment inter-</p> <p>action. We have previously shown that carriers of a longevity-associated variant (LAV) of the BPIFB4 gene enjoy prolonged health</p> <p>spans and lesser cardiovascular complications. Moreover, supplementation of LAV-BPIFB4 via an adeno-associated viral vector im-</p> <p>proves cardiovascular performance in limb ischaemia, atherosclerosis, and diabetes models. Here, we asked whether the LAV-</p> <p>BPIFB4 gene could address the unmet therapeutic need to delay the heart’s spontaneous ageing. </p> <p><strong>Methods and results</strong></p> <p>Immunohistological studies showed a remarkable reduction in vessel coverage by pericytes in failing hearts explanted from elderly patients. This defect was attenuated in patients carrying the homozygous LAV-BPIFB4 genotype. Moreover, pericytes isolated from older hearts showed low levels of BPIFB4, depressed pro-angiogenic activity, and loss of ribosome biogenesis. LAV-BPIFB4 supple- mentation restored pericyte function and pericyte-endothelial cell interactions through a mechanism involving the nucleolar protein nucleolin. Conversely, BPIFB4 silencing in normal pericytes mimed the heart failure pericytes. Finally, gene therapy with LAV-BPIFB4 prevented cardiac deterioration in middle-aged mice and rescued cardiac function and myocardial perfusion in older</p> <p>mice by improving microvasculature density and pericyte coverage.</p> <p><strong>Conclusions</strong></p> <p>We report the success of the LAV-BPIFB4 gene/protein in improving homeostatic processes in the heart’s ageing. These findings open to using LAV-BPIFB4 to reverse the decline of heart performance in older people.</p>
Data set related to the article: "The Longevity-Associated Variant of BPIFB4 Reduces Senescence in Glioma Cells and in Patients' Lymphocytes Favoring Chemotherapy Efficacy"
<p>Abstract: Glioblastoma (GBM) is the most common primary brain cancer with the median age at diagnosis around 64 years, thus pointing to aging as an important risk factor. Indeed, aging, by increasing the senescence burden, is configured as a negative prognostic factor for GBM stage. Furthermore, several anti-GBM therapies exist, such as temozolomide (TMZ) and etoposide (ETP), that unfortunately trigger senescence and the secretion of proinflammatory senescence-associated secretory phenotype (SASP) factors that are responsible for the improper burst of (i) tumorigenesis, (ii) cancer metastasis, (iii) immunosuppression, and (iv) tissue dysfunction. Thus, adjuvant therapies that limit senescence are urgently needed. The longevity-associated variant (LAV) of the bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) gene previously demonstrated a modulatory activity in restoring age-related immune dysfunction and in balancing the low-grade inflammatory status of elderly people. Based on the above findings, we tested LAV- BPIFB4 senotherapeutic effects on senescent glioblastoma U87-MG cells and on T cells from GBM patients. We interrogated SA-β-gal and HLA-E senescence markers, SASP factors, and proliferation and apoptosis assays. The results highlighted a LAV-BPIFB4 remodeling of the senescent phenotype of GBM cells, enhancement of their sensitivity to temozolomide and a selective reduction of the T cells’ senescence from GBM patients. Overall, these findings candidate LAV-BPIFB4 as an adjuvant therapy for GBM.</p>
Higher intelligence is genetically linked with longevity
GEO Series GSE196981. Drosophila melanogaster. 18 samples. Type: Expression profiling by high throughput sequencing.
Efficacy of longevity interventions in C. elegans is determined by early life activity of RNA splicing factors II
GEO Series GSE293218. Caenorhabditis elegans. 40 samples. Type: Expression profiling by high throughput sequencing.
The role of Calment in Drosophila longevity and oxidative stress resistance
GEO Series GSE83605. Drosophila melanogaster. 6 samples. Type: Expression profiling by array.
Data set related to the project RF-2016-02364864 "Exploiting BPIFB4 and its longevity-associated variant in the fight against cardiovascular diseases"
<p>Data set related to the project RF-2016-02364864 "Exploiting BPIFB4 and its longevity-associated variant in the fight against cardiovascular diseases"</p> <p>Background: Maintaining the homeostasis of the vascular system is the prerequisite for delaying cardiovascular diseases (CVDs). In addition to endothelial function, circulating endothelial progenitors (EPCs) number predicts cardiovascular health. We recently discovered a Longevity-Associated Variant of BPIFB4 that modulates endothelial response and EPC mobilization. Of note, serum BPIFB4 levels classify healthy centenarians.</p> <p>Hypothesis: BPIFB4 is a new determinant of cardiovascular health.</p> <p>Specific Aim 1: Demonstrate the association of circulating serum BPIFB4 with atherosclerotic cardiovascular diseases in humans. Verify the additive value of BPIFB4 levels and EPC number in disease prediction.</p> <p>Specific Aim 2: Prove the potential of delivering BPIFB4 recombinant protein in rescuing atherosclerosis in mice.</p> <p>Specific Aim 3: Dissect the molecular mechanisms associated with BPIFB4 activity in EPCs and vascular cells</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.