bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2024‒08‒11
23 papers selected by
Ayesh Seneviratne, Western University
  1. Blocking IL-11 improves healthspan and lifespan in mice.
  2. Regulators of clonal hematopoiesis and physiological consequences of this condition.
  3. Deubiquitinases at the interplay between hematopoietic stem cell aging and myelodysplastic transformation.
  4. Clonal hematopoiesis: malignant implications, extrahematologic manifestations, and management.
  5. Genetic and epigenetic regulation of inflammasomes: Role in atherosclerosis.
  6. Digitising the ageing process with epigenetic clocks.
  7. Frailty in Older Adults.
  8. Nourishing the mind: Fasting for brain health.
  9. Role of the National Institute on Aging in Transforming Aging Research Through Geroscience and Gerotherapeutics-50 Years of Innovation.
  10. Therapy-Induced Cellular Senescence: Potentiating Tumor Elimination or Driving Cancer Resistance and Recurrence?
  11. Geroscience in the continuum from healthy longevity to frailty.
  12. JAK2-mutant Clonal Hematopoiesis is Associated with Venous Thromboembolism.
  13. The Matrix Protein Tropoelastin Prolongs Mesenchymal Stromal Cell Vitality and Delays Senescence During Replicative Aging.
  14. Decline and fall of aging astrocytes: the human perspective.
  15. Clonal hematopoiesis, cardiovascular events and treatment benefit in 63,700 individuals from five TIMI randomized trials.
  16. p16-dependent increase of PD-L1 stability regulates immunosurveillance of senescent cells.
  17. Glycosphingolipid synthesis mediates immune evasion in KRAS-driven cancer.
  18. Why Do We (and Still Do!) Need the National Institute on Aging-50 Years of Innovation.
  19. How the stressed-out brain can weaken the immune system.
  20. Second brain implant by Elon Musk's Neuralink: will it fare better than the first?
  21. Association of the dietary inflammatory index with sarcopenic obesity and frailty in older adults.
  22. Clonal hematopoiesis of indeterminate potential is associated with reduced risk of cognitive impairment in patients with chronic kidney disease.
  23. Mediterranean Diet Linked to Better Heart Health in Children and Teens.
  1. Nat Aging. 2024 Aug 08.
    Blocking IL-11 improves healthspan and lifespan in mice.
    Hannah Walters.
      
    DOI:  https://doi.org/10.1038/s43587-024-00699-9
  2. J Cardiovasc Aging. 2024 Jan;pii: 3. [Epub ahead of print]4(1):
    Regulators of clonal hematopoiesis and physiological consequences of this condition.
    Eunbee Park, Megan A Evans, Kenneth Walsh.
      Clonal hematopoiesis (CH) is a prevalent condition that results from somatic mutations in hematopoietic stem cells. When these mutations occur in "driver" genes, they can potentially confer fitness advantages to the affected cells, leading to a clonal expansion. While most clonal expansions of mutant cells are generally considered to be asymptomatic since they do not impact overall blood cell numbers, CH carriers face long-term risks of all-cause mortality and age-associated diseases, including cardiovascular disease and hematological malignancies. While considerable research has focused on understanding the association between CH and these diseases, less attention has been given to exploring the regulatory factors that contribute to the expansion of the driver gene clone. This review focuses on the association between environmental stressors and inherited genetic risk factors in the context of CH development. A better understanding of how these stressors impact CH development will facilitate mechanistic studies and potentially lead to new therapeutic avenues to treat individuals with this condition.
    Keywords:  Clonal hematopoiesis; aging; genotoxic stress; inflammation
    DOI:  https://doi.org/10.20517/jca.2023.39
  3. FEBS Lett. 2024 Aug 06.
    Deubiquitinases at the interplay between hematopoietic stem cell aging and myelodysplastic transformation.
    Elisabetta Citterio, Antonella Ellena Ronchi.
      Hematopoietic stem cells (HSC) maintain blood production throughout life. Nevertheless, HSC functionality deteriorates upon physiological aging leading to the increased prevalence of haematological diseases and hematopoietic malignancies in the elderly. Deubiquitinating enzymes (DUBs) by reverting protein ubiquitination ensure proper proteostasis, a key process in HSC maintenance and fitness.
    Keywords:  Acute Myeloid Leukemia (AML); Aging; Deubiquitinases; Deubiquitinating enzymes (DUBs); Hematopoietic Stem Cells (HSC); Myelodysplastic Syndromes (MDS); Ubiquitination
    DOI:  https://doi.org/10.1002/1873-3468.14991
  4. Clin Adv Hematol Oncol. 2024 Sep;22(7): 320-327
    Clonal hematopoiesis: malignant implications, extrahematologic manifestations, and management.
    Kelly S Chien, Courtney D DiNardo, Guillermo Garcia-Manero.
      As individuals age, their hematopoietic stem cells can sporadically acquire genetic mutations, known as clonal hematopoiesis. Although most of these genomic aberrations are of little consequence, particular changes in certain contexts can lead to the development of hematologic malignancies, such as myelodysplastic syndromes and acute myeloid leukemia. Owing to its pervasive extrahematologic interactions, clonal hematopoiesis is a recognized risk factor for and is causally implicated in the development of several chronic diseases of aging and/or inflammation, such as atherosclerotic cardiovascular disease. Here, we provide a review of the diagnosis and clinical implications of clonal hematopoiesis, as well as evolving management strategies in the absence of formal consensus guidelines.
  5. Atherosclerosis. 2024 Jul 14. pii: S0021-9150(24)01109-2. [Epub ahead of print]396 118541
    Genetic and epigenetic regulation of inflammasomes: Role in atherosclerosis.
    Mustafa Yalcinkaya, Alan R Tall.
      The cardiovascular complications of atherosclerosis are thought to arise from an inflammatory response to the accumulation of cholesterol-rich lipoproteins in the arterial wall. The positive outcome of CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study) provided key evidence to support this concept and suggested that inflammasomes and IL-1β are important inflammatory mediators in human atherosclerotic cardiovascular diseases (ACVD). In specific settings NLRP3 or AIM2 inflammasomes can induce inflammatory responses in the arterial wall and promote the formation of unstable atherosclerotic plaques. Clonal hematopoiesis (CH) has recently emerged as a major independent risk factor for ACVD. CH mutations arise during ageing and commonly involves variants in genes mediating epigenetic modifications (TET2, DNMT3A, ASXL1) or cytokine signaling (JAK2). Accumulating evidence points to the role of inflammasomes in the progression of CH-induced ACVD events and has shed light on the regulatory pathways and possible therapeutic approaches that specifically target inflammasomes in atherosclerosis. Epigenetic dynamics play a vital role in regulating the generation and activation of inflammasome components by causing changes in DNA methylation patterns and chromatin assembly. This review examines the genetic and epigenetic regulation of inflammasomes, the intersection of macrophage cholesterol accumulation with inflammasome activation and their roles in atherosclerosis. Understanding the involvement of inflammasomes in atherosclerosis pathogenesis may lead to customized treatments that reduce the burden of ACVD.
    Keywords:  AIM2; Atherosclerosis; Epigenetics; Genetics; IL-1β; Inflammasome; NLRP3
    DOI:  https://doi.org/10.1016/j.atherosclerosis.2024.118541
  6. Lancet. 2024 Aug 03. pii: S0140-6736(24)01554-X. [Epub ahead of print]404(10451): 423
    Digitising the ageing process with epigenetic clocks.
    Steve Horvath, Eric J Topol.
      
    DOI:  https://doi.org/10.1016/S0140-6736(24)01554-X
  7. N Engl J Med. 2024 Aug 08. 391(6): 538-548
    Frailty in Older Adults.
    Dae Hyun Kim, Kenneth Rockwood.
      
    DOI:  https://doi.org/10.1056/NEJMra2301292
  8. Cell Metab. 2024 Aug 06. pii: S1550-4131(24)00230-4. [Epub ahead of print]36(8): 1635-1637
    Nourishing the mind: Fasting for brain health.
    Sebastian J Hofer, Frank Madeo.
      Aging and obesity are intertwined in a vicious circle that leads to declining general and brain-specific functions. Kapogiannis and colleagues demonstrate that implementing just 8 weeks of two distinct low-calorie regimes can enhance cognition and biochemical markers of aging in older people with obesity.
    DOI:  https://doi.org/10.1016/j.cmet.2024.06.005
  9. JAMA Intern Med. 2024 Aug 05.
    Role of the National Institute on Aging in Transforming Aging Research Through Geroscience and Gerotherapeutics-50 Years of Innovation.
    John C Newman, Iman M Al-Naggar, George A Kuchel.
      
    DOI:  https://doi.org/10.1001/jamainternmed.2024.2534
  10. Cells. 2024 Jul 30. pii: 1281. [Epub ahead of print]13(15):
    Therapy-Induced Cellular Senescence: Potentiating Tumor Elimination or Driving Cancer Resistance and Recurrence?
    Yue Liu, Isabelle Lomeli, Stephen J Kron.
      Cellular senescence has been increasingly recognized as a hallmark of cancer, reflecting its association with aging and inflammation, its role as a response to deregulated proliferation and oncogenic stress, and its induction by cancer therapies. While therapy-induced senescence (TIS) has been linked to resistance, recurrence, metastasis, and normal tissue toxicity, TIS also has the potential to enhance therapy response and stimulate anti-tumor immunity. In this review, we examine the Jekyll and Hyde nature of senescent cells (SnCs), focusing on how their persistence while expressing the senescence-associated secretory phenotype (SASP) modulates the tumor microenvironment through autocrine and paracrine mechanisms. Through the SASP, SnCs can mediate both resistance and response to cancer therapies. To fulfill the unmet potential of cancer immunotherapy, we consider how SnCs may influence tumor inflammation and serve as an antigen source to potentiate anti-tumor immune response. This new perspective suggests treatment approaches based on TIS to enhance immune checkpoint blockade. Finally, we describe strategies for mitigating the detrimental effects of senescence, such as modulating the SASP or targeting SnC persistence, which may enhance the overall benefits of cancer treatment.
    Keywords:  SASP (senescence-associated secretory phenotype); cancer therapy; immune surveillance; immunosuppression; senescence; senolytics; therapy resistance; tumor microenvironment
    DOI:  https://doi.org/10.3390/cells13151281
  11. Z Gerontol Geriatr. 2024 Aug;57(5): 361-364
    Geroscience in the continuum from healthy longevity to frailty.
    M Cristina Polidori.
      The socioeconomic and technological developments of the past decades have enabled unique progress associated to increased life expectancy and better health for a large part of the world's population; however, multimorbidity, frailty and disability are also on the rise. Geroscience as the new biology of aging is based on the evidence that the main risk factor for noncommunicable chronic diseases (NCD) is the aging process; however, its technology is mostly used for the scientific study of longevity and its interaction with aging medicine and geriatrics is still limited. In this perspective, the need for a tighter exchange between geroscience and geriatrics for longer health span and intrinsic capacity is discussed in the context of existing evidence and knowledge gaps.
    Keywords:  Aging; Frailty; Health span; Life expectancy; Noncommunicable chronic diseases
    DOI:  https://doi.org/10.1007/s00391-024-02331-2
  12. Blood. 2024 Jul 16. pii: blood.2024024187. [Epub ahead of print]
    JAK2-mutant Clonal Hematopoiesis is Associated with Venous Thromboembolism.
    Rebecca L Zon, Aswin Sekar, Katharine Clapham, Ohad Oren, Abhishek Niroula, Alexander G Bick, Christopher J Gibson, Gabriel K Griffin, Md Mesbah Uddin, Donna S Neuberg, Pradeep Natarajan, Benjamin L Ebert.
      Venous thromboembolism (VTE) is common among older individuals, but provoking factors are not identified in many cases. Patients with myeloid malignancies, especially myeloproliferative neoplasms, are at increased risk for venous thrombosis. Clonal hematopoiesis of indeterminate potential (CHIP), a precursor state to myeloid malignancies, is common among the elderly and may similarly predispose to venous thrombosis. We evaluated overall and genotype-specific associations between CHIP and prevalent and incident VTE in >400,000 samples from the UK Biobank. CHIP was modestly associated with incident VTE with a hazard ratio of 1.17 (95% confidence interval (CI) 1.09-1.3; p= 0.002) but was not significantly associated with prevalent VTE with an odds ratio of 1.02 (95% CI 0.81-1.23; p= 0.81). TET2-mutant CHIP was associated with incident VTE with a hazard ratio of 1.33 (95% CI 1.05-1.69; p= 0.02). JAK2 mutations were highly associated with both prevalent and incident VTE risk with odds ratio of 6.58 (95% CI 2.65-16.29; p= 4.7 x 10-5) and hazard ratio of 4.2 (95% CI 2.18-8.08; p= 1.7 x 10-5), respectively, consistent with the thrombophilia associated with JAK2-mutant myeloproliferative neoplasms. The association between JAK2-mutant CHIP and VTE remained significant after excluding potential undiagnosed myeloproliferative neoplasms based on laboratory parameters. Compared to heterozygous factor V Leiden and heterozygous prothrombin gene mutation, JAK2-mutant CHIP was more strongly associated with VTE but was less common. These results indicate that most individuals with CHIP do not have an altered risk of thrombosis, but that individuals with JAK2-mutant CHIP have a significantly elevated risk of VTE.
    DOI:  https://doi.org/10.1182/blood.2024024187
  13. Adv Sci (Weinh). 2024 Aug 09. e2402168
    The Matrix Protein Tropoelastin Prolongs Mesenchymal Stromal Cell Vitality and Delays Senescence During Replicative Aging.
    Sunny Shinchen Lee, Aleen Al Halawani, Jonathan D Teo, Anthony S Weiss, Giselle C Yeo.
      Cellular senescence leads to the functional decline of regenerative cells such as mesenchymal stromal/stem cells (MSCs), which gives rise to chronic conditions and contributes to poor cell therapy outcomes. Aging tissues are associated with extracellular matrix (ECM) dysregulation, including loss of elastin. However, the role of the ECM in modulating senescence is underexplored. In this work, it is shown that tropoelastin, the soluble elastin precursor, is not only a marker of young MSCs but also actively preserves cell fitness and delays senescence during replicative aging. MSCs briefly exposed to tropoelastin exhibit upregulation of proliferative genes and concurrent downregulation of senescence genes. The seno-protective benefits of tropoelastin persist during continuous, long-term MSC culture, and significantly extend the MSC replicative lifespan. Tropoelastin-expanded MSCs further maintain youth-associated phenotype and function compared to age-matched controls, including preserved clonogenic potential, minimal senescence-associated beta-galactosidase activity, maintained cell sizes, reduced expression of senescence markers, suppressed secretion of senescence-associated factors, and increased production of youth-associated proteins. This work points to the utility of exogenously-supplemented tropoelastin for manufacturing MSCs that robustly maintain regenerative potential with age. It further reveals the active role of classical structural ECM proteins in driving cellular age-associated fitness, potentially leading to future interventions for aging-related pathologies.
    Keywords:  aging; fitness; mesenchymal stromal cells; senescence; stem cells; tropoelastin
    DOI:  https://doi.org/10.1002/advs.202402168
  14. Neural Regen Res. 2025 Jun 01. 20(6): 1713-1714
    Decline and fall of aging astrocytes: the human perspective.
    Alexei Verkhratsky, Alexey Semyanov.
      
    DOI:  https://doi.org/10.4103/NRR.NRR-D-24-00418
  15. Nat Med. 2024 Aug 06.
    Clonal hematopoiesis, cardiovascular events and treatment benefit in 63,700 individuals from five TIMI randomized trials.
    Nicholas A Marston, James P Pirruccello, Giorgio E M Melloni, Frederick Kamanu, Marc P Bonaca, Robert P Giugliano, Benjamin M Scirica, Stephen D Wiviott, Deepak L Bhatt, Philippe Gabriel Steg, Itamar Raz, Eugene Braunwald, Peter Libby, Patrick T Ellinor, Alexander G Bick, Marc S Sabatine, Christian T Ruff.
      Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with an increased risk of cardiovascular (CV) disease in the general population. Currently, it is unclear whether this association is observed in large clinical trial cohorts with a high burden of existing CV disease or whether CV therapies can mitigate CHIP-associated CV risk. To address these questions, we studied 63,700 patients from five randomized trials that tested established therapies for CV disease, including treatments targeting the proteins PCSK9, SGLT2, P2Y12 and FXa. During a median follow-up of 2.5 years, 7,453 patients had at least one CV event (CV death, myocardial infarction (MI), ischemic stroke or coronary revascularization). The adjusted hazard ratio (aHR) for CV events for CHIP+ patients was 1.07 (95% CI: 0.99-1.16, P = 0.08), with consistent risk estimates across each component of CV risk. Significant heterogeneity in the risk of MI was observed, such that CHIP+ patients had a 30% increased risk of first MI (aHR = 1.31 (1.05-1.64), P = 0.02) but no increased risk of recurrent MI (aHR = 0.94 (0.79-1.13), Pint = 0.008), as compared to CHIP- patients. Moreover, no significant heterogeneity in treatment effect between individuals with and without CHIP was observed for any of the therapies studied in the five trials. These results indicate that in clinical trial populations, CHIP is associated with incident but not recurrent coronary events and that the presence of CHIP does not appear to identify patients who will derive greater benefit from commonly used CV therapies.
    DOI:  https://doi.org/10.1038/s41591-024-03188-z
  16. Nat Cell Biol. 2024 Aug 05.
    p16-dependent increase of PD-L1 stability regulates immunosurveillance of senescent cells.
    Julia Majewska, Amit Agrawal, Avi Mayo, Lior Roitman, Rishita Chatterjee, Jarmila Sekeresova Kralova, Tomer Landsberger, Yonatan Katzenelenbogen, Tomer Meir-Salame, Efrat Hagai, Ilanit Sopher, Juan-Felipe Perez-Correa, Wolfgang Wagner, Avi Maimon, Ido Amit, Uri Alon, Valery Krizhanovsky.
      The accumulation of senescent cells promotes ageing and age-related diseases, but molecular mechanisms that senescent cells use to evade immune clearance and accumulate in tissues remain to be elucidated. Here we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in ageing and chronic inflammation. We show that p16-mediated inhibition of cell cycle kinases CDK4/6 induces PD-L1 stability in senescent cells via downregulation of its ubiquitin-dependent degradation. p16-expressing senescent alveolar macrophages elevate PD-L1 to promote an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with activating anti-PD-L1 antibodies engaging Fcγ receptors on effector cells leads to the elimination of PD-L1 and p16-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of targeting PD-L1 to improve immunosurveillance of senescent cells and ameliorate senescence-associated inflammation.
    DOI:  https://doi.org/10.1038/s41556-024-01465-0
  17. Nature. 2024 Aug 07.
    Glycosphingolipid synthesis mediates immune evasion in KRAS-driven cancer.
    Mariluz Soula, Gokhan Unlu, Rachel Welch, Aleksey Chudnovskiy, Beste Uygur, Vyom Shah, Hanan Alwaseem, Paul Bunk, Vishvak Subramanyam, Hsi-Wen Yeh, Artem Khan, Søren Heissel, Hani Goodarzi, Gabriel D Victora, Semir Beyaz, Kıvanç Birsoy.
      Cancer cells frequently alter their lipids to grow and adapt to their environment1-3. Despite the critical functions of lipid metabolism in membrane physiology, signalling and energy production, how specific lipids contribute to tumorigenesis remains incompletely understood. Here, using functional genomics and lipidomic approaches, we identified de novo sphingolipid synthesis as an essential pathway for cancer immune evasion. Synthesis of sphingolipids is surprisingly dispensable for cancer cell proliferation in culture or in immunodeficient mice but required for tumour growth in multiple syngeneic models. Blocking sphingolipid production in cancer cells enhances the anti-proliferative effects of natural killer and CD8+ T cells partly via interferon-γ (IFNγ) signalling. Mechanistically, depletion of glycosphingolipids increases surface levels of IFNγ receptor subunit 1 (IFNGR1), which mediates IFNγ-induced growth arrest and pro-inflammatory signalling. Finally, pharmacological inhibition of glycosphingolipid synthesis synergizes with checkpoint blockade therapy to enhance anti-tumour immune response. Altogether, our work identifies glycosphingolipids as necessary and limiting metabolites for cancer immune evasion.
    DOI:  https://doi.org/10.1038/s41586-024-07787-1
  18. JAMA Intern Med. 2024 Aug 05.
    Why Do We (and Still Do!) Need the National Institute on Aging-50 Years of Innovation.
    Kenneth E Covinsky, Lona Mody, Sharon K Inouye.
      
    DOI:  https://doi.org/10.1001/jamainternmed.2024.1326
  19. Nature. 2024 Aug 08.
    How the stressed-out brain can weaken the immune system.
    Sara Reardon.
      
    Keywords:  Brain; Immunology; Microbiome; Neuroscience
    DOI:  https://doi.org/10.1038/d41586-024-02557-5
  20. Nature. 2024 Aug 06.
    Second brain implant by Elon Musk's Neuralink: will it fare better than the first?
    Miryam Naddaf, Liam Drew.
      
    Keywords:  Biotechnology; Brain; Neuroscience
    DOI:  https://doi.org/10.1038/d41586-024-02368-8
  21. BMC Geriatr. 2024 Aug 03. 24(1): 654
    Association of the dietary inflammatory index with sarcopenic obesity and frailty in older adults.
    Sukyoung Jung, Yunhwan Lee, Kirang Kim, Sohyun Park.
      OBJECTIVES: This study examined whether a higher dietary inflammatory index (DII®) is associated with the risk of sarcopenic obesity (SO) and frailty among Korean older adults.METHODS: A total of 950 participants aged 70-84 years, who completed the baseline nutrition survey of the Korean Frailty and Aging Cohort Study, were included in the analysis. The DII, quantifying the dietary inflammatory potential, was calculated using 23 foods and nutrients as assessed by a 24-h dietary recall. SO was defined as the coexistence of sarcopenia (dual-energy X-ray absorptiometry-measured appendicular skeletal muscle mass index of < 7.0 for males; <5.4 for females) and abdominal obesity (waist circumference of ≥ 90 cm for males; ≥85 cm for females). Frailty status was assessed using the Fried frailty index (range, 0-5), a simple tool for defining frailty that consists of three or more of five frailty items. Multinomial logistic regression models were used to estimate odds ratios (ORs) with 95% confidence intervals (CIs), adjusting for confounders.
    RESULTS: The prevalence of SO and frailty was 9.8% and 10.8%, respectively. The DII was significantly higher in the frail group (2.7) compared to the robust and SO groups (2.0 vs. 1.8) (P < 0.001). Among nutrients and foods included in the DII, the frail group exhibited lower vitamin E, niacin, vitamin B6, energy, and protein intakes than the robust and SO groups. Multivariable-adjusted OR (95% CI) for frailty versus robust (comparing DII tertile 3 to tertile 1) was 2.3 (1.1-4.8; P-trend = 0.02). However, no significant association was observed between the DII and SO (OR, 1.1; 95% CI, 0.5-2.1; P-trend = 0.6).
    CONCLUSIONS: A higher DII score was associated with increased odds of frailty but not with SO in Korean older adults, suggesting that proinflammatory diets have a greater impact on frailty than that on SO in the older population.
    Keywords:  Aging; Dietary inflammatory index; Frailty; Korean older adults; Sarcopenic obesity
    DOI:  https://doi.org/10.1186/s12877-024-05239-z
  22. Alzheimers Dement. 2024 Aug 08.
    Clonal hematopoiesis of indeterminate potential is associated with reduced risk of cognitive impairment in patients with chronic kidney disease.
    CRIC Study Investigators
      INTRODUCTION: Clonal hematopoiesis of indeterminate potential (CHIP) and dementia disproportionately burden patients with chronic kidney disease (CKD). The association between CHIP and cognitive impairment in CKD patients is unknown.METHODS: We conducted time-to-event analyses in up to 1452 older adults with CKD from the Chronic Renal Insufficiency Cohort who underwent CHIP gene sequencing. Cognition was assessed using four validated tests in up to 6 years mean follow-up time. Incident cognitive impairment was defined as a test score one standard deviation below the baseline mean.
    RESULTS: Compared to non-carriers, CHIP carriers were markedly less likely to experience impairment in attention (adjusted hazard ratio [HR] [95% confidence interval {CI}] = 0.44 [0.26, 0.76], p = 0.003) and executive function (adjusted HR [95% CI] = 0.60 [0.37, 0.97], p = 0.04). There were no significant associations between CHIP and impairment in global cognition or verbal memory.
    DISCUSSION: CHIP was associated with lower risks of impairment in attention and executive function among CKD patients.
    HIGHLIGHTS: Our study is the first to examine the role of CHIP in cognitive decline in CKD. CHIP markedly decreased the risk of impairment in attention and executive function. CHIP was not associated with impairment in global cognition or verbal memory.
    Keywords:  CHIP; attention; chronic kidney disease; clonal hematopoiesis of indeterminate potential; cognitive impairment; executive function; trail making tests
    DOI:  https://doi.org/10.1002/alz.14182
  23. JAMA. 2024 Aug 09.
    Mediterranean Diet Linked to Better Heart Health in Children and Teens.
    Samantha Anderer.
      
    DOI:  https://doi.org/10.1001/jama.2024.14877
This page is being maintained by Thomas Krichel. It was last updated on 2024‒09‒22 at 13:38.