Neuroplasticity, the brain's capacity to adapt and reorganize in response to experiences and environmental changes, is fundamental to cognitive aging. As individuals age, cognitive functions such as m Show more
Neuroplasticity, the brain's capacity to adapt and reorganize in response to experiences and environmental changes, is fundamental to cognitive aging. As individuals age, cognitive functions such as memory, processing speed, and executive function commonly decline, driven largely by changes in neuroplasticity mechanisms like synaptic plasticity, neurogenesis, and functional reorganization. Synaptic plasticity is a well-established mechanism supporting learning and memory across the lifespan, whereas adult neurogenesis, robustly demonstrated in rodents, remains highly limited and controversial in the adult and aged human brain, with evidence largely restricted to rare post-mortem observations and injury-associated conditions. Functional reorganization allows the brain to adapt to structural changes, helping to preserve cognitive function despite age-related decline. Several factors, including oxidative stress, neuroinflammation, and hormonal shifts, exacerbate the decline in neuroplasticity, accelerating cognitive deterioration. Various interventions, including cognitive training, physical exercise, and pharmacological approaches, have demonstrated the potential to promote neuroplasticity and support cognitive health in aging populations. However, one of the major challenges is tailoring these interventions to the unique needs of individuals, as well as identifying novel therapeutic targets for intervention. To effectively address the cognitive decline associated with aging, future research should focus on developing personalized strategies and innovative techniques to enhance or modulate specific neuroplasticity-related processes under defined conditions in the aging brain. These advancements may provide better tools for delaying, mitigating, or even reversing age-related cognitive decline, improving quality of life for older individuals. Show less
Endometriosis is a condition in which functional endometrial glands and stroma are found to grow outside the uterine cavity that can lead to symptoms like dysmenorrhea, dyspareunia, adhesions, and inf Show more
Endometriosis is a condition in which functional endometrial glands and stroma are found to grow outside the uterine cavity that can lead to symptoms like dysmenorrhea, dyspareunia, adhesions, and infertility. Current treatment strategies can provide only symptomatic relief as its etiology remains unclear. Several studies have linked the cellular process of epithelial-mesenchymal transition (EMT) to endometriosis development; however, what triggers EMT states in endometriosis is unknown. Polycomb group (PcG) proteins are histone modifiers that control gene expression by catalyzing repressive histone modifications such as H3K27me3/2 and H2AK119ub1. The misexpression of PcGs and/or genes controlled by them reportedly causes several types of cancers, such as breast, colon, pancreatic, and liver. We investigated whether dysregulation of PcG proteins such as RING1B, BMI1, and EZH2 in ectopic endometriotic tissue as compared to eutopic correlates with genes required for EMT in endometriotic tissue from the same patient with laparoscopically confirmed endometriosis. We quantified the expression of Polycomb repressive complex 1 (PRC1) genes (RING1B and BMI1), EMT-associated genes (TWIST, SNAI1, SNAI2, ZEB1, CDH1, CDH2, and VIM) in paired eutopic and ectopic (endometriotic) tissue samples obtained from 12 women who underwent laparoscopy for severe endometriosis identified as per #ENZIAN classification. Our results showed that the endometriotic lesions had higher gene expression of PRC1 proteins - RING1B and BMI1 as well as higher expression of EMT associated genes than the endometrial tissue. Thus, our results suggest that PRC1 proteins may have a role in the pathogenesis of endometriosis. Show less