Chronic Diseases and Translational Medicine最新文献

Monoclonal antibodies (mAbs) have made significant progress in the treatment of Alzheimer's disease (AD). However, mAbs are associated with adverse effects, including Amyloid-Related Imaging Abnormality (ARIA), which manifests as edema or effusion (ARIA-E) and hemorrhage (ARIA-H). The mechanisms behind these effects are not yet fully understood. Moreover, spontaneous ARIA has been insufficiently explored, and mAb therapies, particularly lecanemab, have mainly focused on patients with the APOE-ε4 allele carrier. This review aims to address this gap by examining the mechanisms of spontaneous ARIA, ARIA induced by mAbs, and the influence of genetic variants on ARIA development. The autoantibody-Aβ-mediated immune response targets excessive Aβ deposits, increasing immune activity through microglial reactivity. The heightened immune response, driven by Aβ accumulation in blood vessels, promotes angiopathy and inflammation, potentially contributing to spontaneous ARIA. The APOE-ε4 allele carrier is more strongly associated with ARIA-E because it redistributes Aβ deposition from the brain to blood vessels, influencing microglial reactivity. The redistribution enhances vascular integrity and reduces the risk of ARIA-H. However, it also increases the likelihood of ARIA-E due to Aβ accumulation in the vasculature, triggering inflammation. In contrast, the development of ARIA-H is linked to increased TREM2 expression and microglial reactivity, leading to impaired vascular integrity and disrupted matrix remodeling, which worsens the condition. Additionally, the adverse effects of mAbs may extend beyond the APOE-ε4 allele, possibly impacting other genetic variants involved in microglial reactivity, Aβ redistribution, and vascular integrity.

The prevalence of renal diseases and its associated burden on healthcare have tremendously risen in the past few years. From simple markers assessing kidney function, current renal research delves into understanding the diseases at the cellular and molecular levels and not just at treating, but at improving quality of life, arresting progression and providing personalized diagnostics and therapy. This narrative review highlights the improvements in diagnostic applications of kidney disease and briefly discusses a few notable biomarkers emphasizing the high throughput omics technologies, as well as contemporary perspectives on renal research. A thorough literature search was performed on PubMed, Scopus, Web of Science, and Medline. Suitable Mesh terms were included for the search strategy, and relevant evidence was documented. Language models and pharmacognosy, along with other omics strategies, impose a better understanding of the renal disease, and the remarkable discoveries of noninvasive biomarkers, urine 273-peptide classifier, and urine peptides-based fibrosis classifier have unraveled the associations between mechanistic studies and novel therapeutic drugs. Strides in biomarker research have been able to delineate stages and types with superior specificity and sensitivity, thereby providing a better diagnosis. Renal research reflects a powerful, dynamic, and multifaceted field that drives better advancements and discoveries in personalized medicine, drug interventions, and patient-centered outcomes. Understanding the tangled relationship of the etiology of kidney disease, these developments and future research hold promise for individuals affected by kidney diseases

S. Lehrer and P. H. Rheinstein, “Alignment of Human Aquaporin 4 and ß-Amyloid Proteins May Indicate Involvement of ß-Amyloid in Brain Water Homeostasis and Prevention of Brain Edema,” Chronic Diseases and Translational Medicine 9 (2023): 177–181. https://doi.org/10.1002/cdt3.64.

The original article included a Conflict of Interest statement which stated: “The authors declare no conflicts of interest.” The journal and the publisher have determined that a conflict of interest on behalf of each author was not declared at publication. The journal and the publisher have had sufficient communication with the authors via email after raising questions about the Conflict of Interest in the article. The authors declared that there was no undeclared Conflict of Interest and further stated that their individual affiliations with commercial entities did not influence the research findings. Following further correspondence between the publisher and the authors, all parties have agreed to include the following Conflicts of Interest statement with the published article.

Steven Lehrer serves in a scientific advisory capacity with Fermata Pharma Inc. Peter H. Rheinstein is President of Severn Health Solutions. The scientific content was developed without influence from Fermata Pharma Inc. or Severn Health Solutions.

S. Lehrer and P. H. Rheinstein, “Alignment of Human KAT2A (GCN5) Histone Acetyltransferase and SARS-CoV-2 Orf8 Viral Proteins,” Chronic Diseases and Translational Medicine 9 (2023): 263–265. https://doi.org/10.1002/cdt3.56.

The original article included a Conflict of Interest statement which stated: “The authors declare no conflicts of interest.” The journal and the publisher have determined that a conflict of interest on behalf of each author was not declared at publication. The journal and the publisher have had sufficient communication with the authors via email after raising questions about the Conflict of Interest in the article. The authors declared that there was no undeclared Conflict of Interest and further stated that their individual affiliations with commercial entities did not influence the research findings. Following further correspondence between the publisher and the authors, all parties have agreed to include the following Conflicts of Interest statement with the published article:

Steven Lehrer serves in a scientific advisory capacity with Fermata Pharma Inc. Peter H. Rheinstein is President of Severn Health Solutions. The scientific content was developed without influence from Fermata Pharma Inc. or Severn Health Solutions.

Echocardiography showed the myocardial ischemia presentation of an 8-month-old boy.