Aging brain最新文献

Tau aggregation induces cell death in iPSC-derived neurons Tau 聚集诱导 iPSC 衍生神经元的细胞死亡

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100136

Hirokazu Tanabe , Sumihiro Maeda , Etsuko Sano , Norio Sakai , Setsu Endoh-Yamagami , Hideyuki Okano

{"title":"Tau aggregation induces cell death in iPSC-derived neurons","authors":"Hirokazu Tanabe , Sumihiro Maeda , Etsuko Sano , Norio Sakai , Setsu Endoh-Yamagami , Hideyuki Okano","doi":"10.1016/j.nbas.2025.100136","DOIUrl":"10.1016/j.nbas.2025.100136","url":null,"abstract":"<div><div>Abnormal accumulation of tau proteins in the brain is a hallmark of neurodegenerative diseases such as Alzheimer’s disease and is closely linked with neuronal cell death. Tau accumulation is a prominent therapeutic target for Alzheimer’s disease, since tau accumulation correlates well with the disease progression, and tau-targeting drugs hold potentials to halt the disease progression. Given the differential response of human and mouse neuronal cells, there is a critical need for a human cellular platform to quickly screen for tau-related neurodegenerative disease therapeutics. However, inducing rapid, tau-dependent neuronal cell death in human models remains challenging. In this study, we established a human cellular model capable of inducing tau aggregation-dependent neuronal cell death within two weeks via tau overexpression. Additionally, we demonstrated the neuroprotective efficacy of known tau-targeting compounds within this system. These findings suggest that our cellular model recapitulates the molecular pathogenesis of tau-induced neurodegeneration and could serve as a valuable platform for drug screening in tauopathies.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100136"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816765","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}

引用次数: 0

Frontal theta oscillations and cognitive flexibility: Age-related modulations in EEG activity 额叶θ波振荡与认知灵活性：脑电图活动的年龄相关调节

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100142

Margarita Darna , Christopher Stolz , Hannah-Sophia Jauch , Hendrik Strumpf , Jens-Max Hopf , Constanze I. Seidenbecher , Björn H. Schott , Anni Richter

{"title":"Frontal theta oscillations and cognitive flexibility: Age-related modulations in EEG activity","authors":"Margarita Darna , Christopher Stolz , Hannah-Sophia Jauch , Hendrik Strumpf , Jens-Max Hopf , Constanze I. Seidenbecher , Björn H. Schott , Anni Richter","doi":"10.1016/j.nbas.2025.100142","DOIUrl":"10.1016/j.nbas.2025.100142","url":null,"abstract":"<div><div>Cognitive flexibility, the ability to adapt one’s behaviour in changing environments, declines during aging. Electroencephalography (EEG) studies have implicated midfrontal theta oscillations in attentional set-shifting, a measure of cognitive flexibility. Little is known about the electrocortical underpinnings of set-shifting in aging. Here, we investigated aging effects on set-shifting performance by analysing theta power in 20 young (mean age: 22.5 ± 2.9 years) and 19 older (mean age: 69.4 ± 6.1 years) adults. Increasing shift difficulty (i.e., intra- vs. extra-dimensional shifts) elicited worse performance in both age groups, with older adults showing overall longer reaction times (RTs) and increased RT variability. Young adults exhibited amplified midfrontal theta power increases with higher shift difficulty whereas older adults showed overall lower theta power and no task-related midfrontal theta power modulation, indicating potentially distinct underlying neural mechanisms.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"8 ","pages":"Article 100142"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365585","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}

引用次数: 0

TOMM40 may mediate GFAP, neurofilament light Protein, pTau181, and brain morphometry in aging TOMM40可能在衰老过程中介导GFAP、神经丝轻蛋白、pTau181和脑形态计量学。

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2024.100134

Robyn A. Honea , Heather Wilkins , Suzanne L. Hunt , Paul J. Kueck , Jeffrey M. Burns , Russell H. Swerdlow , Jill K. Morris

{"title":"TOMM40 may mediate GFAP, neurofilament light Protein, pTau181, and brain morphometry in aging","authors":"Robyn A. Honea , Heather Wilkins , Suzanne L. Hunt , Paul J. Kueck , Jeffrey M. Burns , Russell H. Swerdlow , Jill K. Morris","doi":"10.1016/j.nbas.2024.100134","DOIUrl":"10.1016/j.nbas.2024.100134","url":null,"abstract":"<div><div>A growing amount of data has implicated the <em>TOMM40</em> gene in the risk for Alzheimer’s disease (AD), neurodegeneration, and accelerated aging. No studies have investigated the relationship of <em>TOMM40</em> rs2075650 (‘650<em>)</em> on the structural complexity of the brain or plasma markers of neurodegeneration. We used a comprehensive approach to quantify the impact of <em>TOMM40</em> ‘650 on brain morphology and multiple cortical attributes in cognitively unimpaired (CU) individuals. We also tested whether the presence of the risk allele, G, of <em>TOMM40</em> ‘650 was associated with plasma markers of amyloid, tau, and neurodegeneration and if there were interactions with age and sex, controlling for the effects of <em>APOE</em> ε4. We found that the <em>TOMM40</em> ‘650 G-allele was associated with decreased sulcal depth, increased gyrification index, and decreased gray matter volume. NfL, GFAP, and pTau181 had independent and age-associated increases in individuals with a G-allele. Our data suggest that <em>TOMM40</em> ‘650 is associated with aging-related plasma biomarkers and brain structure variation in temporal-limbic circuits.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100134"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933794","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}

引用次数: 0

Testing the causal impact of plasma amyloid on total Tau using a genetically informative sample of adult male twins 使用成年男性双胞胎的遗传信息样本测试血浆淀粉样蛋白对总Tau蛋白的因果影响

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100139

Nathan A. Gillespie , Michael C. Neale , Matthew S. Panizzon , Ruth E. McKenzie , Xin M. Tu , Hong Xian , Chandra A. Reynolds , Michael J. Lyons , Robert A. Rissman , Jeremy A. Elman , Carol Franz , William S. Kremen

{"title":"Testing the causal impact of plasma amyloid on total Tau using a genetically informative sample of adult male twins","authors":"Nathan A. Gillespie , Michael C. Neale , Matthew S. Panizzon , Ruth E. McKenzie , Xin M. Tu , Hong Xian , Chandra A. Reynolds , Michael J. Lyons , Robert A. Rissman , Jeremy A. Elman , Carol Franz , William S. Kremen","doi":"10.1016/j.nbas.2025.100139","DOIUrl":"10.1016/j.nbas.2025.100139","url":null,"abstract":"<div><div>The amyloid cascade hypothesis predicts that amyloid-beta (Aβ) aggregation drives tau tangle accumulation. We tested competing causal and non-causal hypotheses regarding the direction of causation between Aβ40 and Aβ42 and total Tau (t-Tau) plasma biomarkers. Plasma Aβ40, Aβ42, t-Tau, and neurofilament light chain (NFL) were measured in 1,035 men (mean = 67.0 years) using Simoa immunoassays. Genetically informative twin modeling tested the direction of causation between Aβs and t-Tau. No clear evidence that Aβ40 or Aβ42 directly causes t-Tau was observed. Instead, the alternative causal hypotheses also fit the data well. In contrast, exploratory analyses suggested a causal impact of the Aβ biomarkers on NFL. Separately, reciprocal causation was observed between t-Tau and NFL. Plasma Aβ40 or Aβ42 do not appear to have a direct causal impact on t-Tau, though our use of total rather than phosphorylated tau was a limitation. In contrast, Aβ biomarkers appeared to causally impact NFL in cognitively unimpaired men in their late 60 s.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100139"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144071353","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}

引用次数: 0

No sex differences in the association between regional brain structure abnormalities and cognitive functioning in a geriatric memory clinic population 在老年记忆临床人群中，区域脑结构异常和认知功能之间的关联没有性别差异

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100137

A. Lamé , E.G. Thomas , S.A.J. van de Schraaf , C. Groot , C.H. Sudre , F. Barkhof , M. Muller , R. Ossenkoppele , H.F.M. Rhodius-Meester

{"title":"No sex differences in the association between regional brain structure abnormalities and cognitive functioning in a geriatric memory clinic population","authors":"A. Lamé , E.G. Thomas , S.A.J. van de Schraaf , C. Groot , C.H. Sudre , F. Barkhof , M. Muller , R. Ossenkoppele , H.F.M. Rhodius-Meester","doi":"10.1016/j.nbas.2025.100137","DOIUrl":"10.1016/j.nbas.2025.100137","url":null,"abstract":"<div><div>Differences between men and women in cognitive impairment and neurodegeneration are not yet well understood. Although sex differences in brain structure abnormalities, including white matter hyperintensities (WMH) and grey matter (GM) atrophy, have been associated with cognitive decline in the ageing population, the evidence is limited and inconclusive. Therefore, we explored sex differences in brain structure abnormalities and in the association between brain structure abnormalities and cognitive functioning. We analyzed global and regional volumetric measures of WMH and GM of 475 patients visiting an academic geriatric memory clinic in the Netherlands with multiple linear regression analyses. For both global and regional WMH and GM, we found no sex differences in brain structure abnormalities. We also found no interaction of sex on the association between brain structure abnormalities and cognitive functioning. We reflect on using a binary classification of men and women based on sex in this study, which might overlook individual differences and does not elucidate gender-related factors that influence health and risk of pathology. Future studies should focus on exploring the relationship between sex and gender on brain structure and cognitive functioning beyond this binary model, by including more data on social context, more diverse populations and using intersectional approaches.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100137"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143902418","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}

引用次数: 0

Complex span measures of working memory do not mediate the effects of age on the P3 and N400 ERPs 工作记忆的复杂广度测量不介导年龄对P3和N400 erp的影响

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100140

Jasmin Joshi, Chandlyr M. Denaro, Alan A. Hartley, Catherine L. Reed

{"title":"Complex span measures of working memory do not mediate the effects of age on the P3 and N400 ERPs","authors":"Jasmin Joshi, Chandlyr M. Denaro, Alan A. Hartley, Catherine L. Reed","doi":"10.1016/j.nbas.2025.100140","DOIUrl":"10.1016/j.nbas.2025.100140","url":null,"abstract":"<div><div>Working memory (WM), the temporary maintenance of a limited amount of information in an accessible state, is required for the performance of many tasks. Studies have shown that WM demands are related to the neural processing of tasks requiring attention: Age affects the ERP components associated with WM context updating processes in the visual oddball task (P3) and semantic processing in the word-pair judgment task (N400). This study investigated whether WM capacity measured by complex span tasks mediates the effects of age on these ERPs. Younger adults (YA, n = 44, ages 18–23 yr) and older adults (OA, n = 41, ages 69–89 yr) completed operation, reading, and symmetry complex span tasks and two ERP tasks (P3/visual oddball; N400/word-pair judgment). Results showed age-related differences for all complex span tests. Principal components analysis of these tests showed a single factor for both groups, so a combined WM capacity factor score was created. Regressions of age group and WM factor score on P3 and N400 amplitudes and latencies showed that OAs had relatively lower amplitudes and longer latencies. However complex span was not related to P3 or N400 amplitudes or latencies and that result was the same for younger and older adults; that is, complex span did not mediate the age effects. WM processes indexed by the P3 and N400 components appear to be different from those elicited by complex span tasks. Attentional control processes of WM influence oddball and semantic judgement tasks more than storage components.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100140"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922898","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}

引用次数: 0

Selenium deficiency negatively affects survival and integrity of human hippocampal progenitor cells 缺硒对人海马祖细胞的存活和完整性有负面影响

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100138

Sahand Farmand, Emaan Ahmed, Hadisa Azizi Zawar, Sandrine Thuret

{"title":"Selenium deficiency negatively affects survival and integrity of human hippocampal progenitor cells","authors":"Sahand Farmand, Emaan Ahmed, Hadisa Azizi Zawar, Sandrine Thuret","doi":"10.1016/j.nbas.2025.100138","DOIUrl":"10.1016/j.nbas.2025.100138","url":null,"abstract":"<div><div>Selenium has been shown to be a key regulatory element in the health, survival and proliferation of neural stem and progenitor cells, with various studies underlining its anti-aging properties. However, most of this knowledge is derived from rodent models, leaving its effects on human hippocampal progenitor cells unclear. In this study, we utilized a human hippocampal progenitor cell (HPC) line to examine the effects of varying concentrations of sodium selenite, an inorganic form of selenium (0 µM, 0.1 µM, 0.23 µM, 0.5 µM, and 1.0 µM), on the proliferation, apoptosis, and progenitor integrity of these cells. To do this, HPCs were exposed to these concentrations for 48 h, followed by immunocytochemistry to quantify, cell number (DAPI-positive cells), proliferation (KI67-positve cells), apoptosis (CC3-positve cells), and progenitor integrity (SOX2- and Nestin-positive cells). While our results indicated no significant effects of selenium concentrations on proliferation or apoptosis, we demonstrated that absence of selenium (0 μM) in the culture media significantly reduced both cell number and percentage of Nestin-positive cells, but only when compared to the condition with the highest selenium concentration (1.0 μM). Our findings underscore the role of selenium in regulating the survival and integrity of human HPCs. Lastly, we emphasize the need for further research to uncover the mechanisms underlying these observed changes.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100138"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891489","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}

引用次数: 0

Cellular senescence, neuroinflammation, and microRNAs: Possible interactions driving aging and neurodegeneration in the hippocampal neurogenic niche 细胞衰老、神经炎症和microrna：海马神经源性生态位中驱动衰老和神经变性的可能相互作用

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100141

O. Polzer , E. Kinloch , C.P. Fitzsimons

引用次数: 0

Nigrostriatal dopaminergic neurotransmission and resilience to peripheral systemic risk factors for gait slowing upon transition to uneven surfaces in older adult 黑质纹状体多巴胺能神经传递和对周围系统危险因素的恢复能力在老年人过渡到不平整的表面时步态减慢

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100143

Lana M. Chahine , Andrea Rosso , Ian Troidl , Mary Ganguli , Anne Newman , Steven Cummings , Stephanie Studenski , Brian Lopresti , Sarah Royse , Theodore Huppert , Mark Redfern , Patrick J. Sparto , Nico I. Bohnen , Caterina Rosano

{"title":"Nigrostriatal dopaminergic neurotransmission and resilience to peripheral systemic risk factors for gait slowing upon transition to uneven surfaces in older adult","authors":"Lana M. Chahine , Andrea Rosso , Ian Troidl , Mary Ganguli , Anne Newman , Steven Cummings , Stephanie Studenski , Brian Lopresti , Sarah Royse , Theodore Huppert , Mark Redfern , Patrick J. Sparto , Nico I. Bohnen , Caterina Rosano","doi":"10.1016/j.nbas.2025.100143","DOIUrl":"10.1016/j.nbas.2025.100143","url":null,"abstract":"<div><div>Identifying mechanisms that compensate for slow gait speed in older adults is crucial. Dopaminergic neurotransmission curbs deleterious associations of cerebrovascular disease with gait, but whether it compensates for peripheral systemic risk factors (PSRF) for gait slowing has not been studied. In this cross-sectional study of community-dwelling older adults, we examined the relationship between nigrostriatal dopaminergic terminal integrity and gait speed in individuals with and without ≥ 1 PSRF for gait slowing: obesity, joint pain, or reduced muscle strength. The primary outcome was gait speed cost (%GSC) on transition from even to uneven surface. Participants underwent dopaminergic imaging with dihydrotetrabenazine [<sup>11</sup>C]DTBZ positron emission tomography. Among 197 individuals, (mean (SD) age 74.92 (4.53) years; 61.93 % female; 90.86 % White), 130 (65.99 %) had ≥ 1 PSRF. Relationship between posterior putamen [<sup>11</sup>C]DTBZ binding and %GSC was modified by PSRF; in those with ≥ 1 PSRF (but not in those with no PSRF), posterior putamen [<sup>11</sup>C]DTBZ binding was associated with %GSC (β = 0.198, p = 0.03) independent of potential confounders. This cross-sectional study indicates that higher striatal dopaminergic neurotransmission may compensate for the effects of PSRF on gait slowing.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"8 ","pages":"Article 100143"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330520","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}

引用次数: 0

Effects of global Ripk2 genetic deficiency in aged mice following experimental ischemic stroke Ripk2基因缺失对实验性缺血性脑卒中老年小鼠的影响

IF 1.7

Aging brain Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100135

John Aaron Howell , Jonathan Larochelle , Rachel E. Gunraj , Sofia M. Stansbury , Lei Liu , Changjun Yang , Eduardo Candelario-Jalil

{"title":"Effects of global Ripk2 genetic deficiency in aged mice following experimental ischemic stroke","authors":"John Aaron Howell , Jonathan Larochelle , Rachel E. Gunraj , Sofia M. Stansbury , Lei Liu , Changjun Yang , Eduardo Candelario-Jalil","doi":"10.1016/j.nbas.2025.100135","DOIUrl":"10.1016/j.nbas.2025.100135","url":null,"abstract":"<div><div>Besides the loss of blood and oxygen reaching the ischemic tissue, many secondary effects of ischemic stroke can cause additional tissue damage, including inflammation, oxidative stress, and proteomic disturbances. Receptor-interacting serine/threonine kinase 2 (RIPK2) is an important mediator in the post-stroke inflammatory cascade that responds to signals and molecular patterns released by dead or dying cells in the ischemic area. We hypothesize that RIPK2 signaling worsens injury and neurological recovery post-stroke and that global deletion of <em>Ripk2</em> is protective following ischemic stroke in aged mice. Aged (18–24 months) male mice were subjected to permanent middle cerebral artery occlusion (pMCAO). Vertical grid, weight grip, and open field were conducted at baseline and on days 1, 2, 3, 8, 15, and 22 post-stroke. Cognitive tests (novel object recognition and Y-maze) were performed at baseline and day 28 post-stroke. Infarct size was measured using cresyl violet staining, and reactive gliosis was measured using Iba1 and GFAP staining at day 28 post-stroke. Global deletion of <em>Ripk2</em> (<em>Ripk2<sup>-/-</sup></em>) in aged mice resulted in smaller infarct volume and improved performance on vertical grid and weight grip tests compared to aged wildtype (WT) mice. Additionally, aged <em>Ripk2</em><sup>-/-</sup> mice had less Iba1 staining in the ipsilateral cortex than the aged WT control mice. This study further elucidates the role of RIPK2 signaling in the ischemic cascade and expands our knowledge of RIPK2 in stroke to aged mice. These results support the hypothesis that RIPK2 signaling worsens injury post-stroke and may be an attractive candidate for therapeutic intervention.</div></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"7 ","pages":"Article 100135"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143734808","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}

引用次数: 0