Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairments that might be accompanied by declines in activities of daily living, neuropsychiatric disorders and a loss of motor function [1,2]. At present, the prevalence of dementia of Alzheimer’s type (DAT) is approximately 4% among elderly people [3]. With the increase in the aging the population, the number of individuals with DAT is still increasing.

The promising results of immune checkpoint inhibitors (ICIs) in tumors have changed the current treatment modality for cancer. ICIs response prediction is urgently needed for the personalized therapy approach. In the recent issue of the Journal of Oncology, Zixin Hu et al. proposed that DNA methylation alternations contribute to tumor microenvironment (TME) reshapement to predict the ICIs response. Notwithstanding the global DNA methylation loss, the repression of T cell receptor signaling and the fellow costimulators by DNA hypermethylation contributed to the cold TME and ICIs resistance.

This study presents a comprehensive exploration into the shared molecular mechanisms linking psoriasis and major depressive disorder (MDD), two conditions that are increasingly recognized as having potential comorbidities. It offers new insights into the immune and genetic pathways that may contribute to both disorders, emphasizing the potential of CD19 as a biomarker and therapeutic target through the PPARγ/β-catenin/Wnt3a signaling pathway.

Epigenetics is the study of heritable modifications to gene expression, such as DNA methylation, histone modifications, and RNA modifications, that do not alter the nucleotide sequence of the corresponding gene. Recently, RNA modification has emerged as a novel research focus. We have detected over 170 different RNA modifications,  such as N6-methyladenosine (m6A), N7-methylguanosine (m7G), 5-methylcytosine (m5C), N1-methyladenosine (m1A), N3-methylcytosine (m3C), and pseudouridine (ψ).These modifications are important for biological processes like RNA metabolism and post-transcriptional regulation. 

In prior work, we analyzed gene expression profiles of mouse, rat and human gastrocnemius muscles to identify conserved regulators of muscle aging processes. By further comparing data obtained from different muscles we found stronger conservation of aging-related factors at the level of molecular pathways than at the level of individual genes.