CNS tumours occur in both pediatric and adult patients and many of these tumours are associated with poor clinical outcome. Due to a paradigm shift in thinking for the last several years, these tumours are now considered to originate from a small population of stem-like cells within the bulk tumour tissue. These cells, termed as brain tumour initiating cells (BTICs), are perceived to be regulated by microRNAs at the posttranscriptional/translational levels. Proliferation, stemness, differentiation, invasion, angiogenesis, metastasis, apoptosis, and cell cycle constitute some of the significant processes modulated by microRNAs in cancer initiation and progression. Characterization and functional studies on oncogenic or tumour suppressive microRNAs are made possible because of developments in sequencing and microarray techniques. In the current review, we bring recent knowledge of the role of microRNAs in BTIC formation and therapy. Special attention is paid to two highly aggressive and well-characterized brain tumours: gliomas and medulloblastoma. As microRNA seems to be altered in the pathogenesis of many human diseases, "microRNA therapy" may now have potential to improve outcomes for brain tumour patients. In this rapidly evolving field, further understanding of miRNA biology and its contribution towards cancer can be mined for new therapeutic tools.
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http://dx.doi.org/10.1155/2015/141793 | DOI Listing |
Alzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA; NYU, New York City, NY, USA.
Background: Astrocytes, a major glial cell in the central nervous system (CNS), can become reactive in response to inflammation or injury, and release toxic factors that kill specific subtypes of neurons. Over the past several decades, many groups report that reactive astrocytes are present in the brains of patients with Alzheimer's disease, as well as several other neurodegenerative diseases. In addition, reactive astrocyte sub-types most associated with these diseases are now reported to be present during CNS cancers of several types.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Afe Babalola University, Ado-Ekiti (ABUAD), Ado-Ekiti, Ekiti state, Nigeria.
Background: The impact of probiotics as gut and immunological modulator in restoring gut microbial balance and immune cells expression have generated much attention in the health sector. Its inhibitory effect on bacterial translocation and associated neural inflammatory processes has been reported. However, there is scarcity of data on its neuroprotective impact against neuroinflammation-associated neurodegeneration and memory impairment.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The TT & WF Chao Center for BRAIN and Houston Methodist Neal Cancer Center, Houston Methodist Hospital, Houston, TX, USA.
Background: Global epidemiological studies involving over nine million participants have shown a 35% lower incidence of Alzheimer's Disease (AD) in older cancer survivors compared to those without a history of cancer. This inverse relationship, consistent across recent studies with methodological controls, suggests that cancer itself, rather than cancer treatments, may offer protective factors against AD. This insight opens avenues for novel therapeutic strategies targeting early AD by harnessing cancer-associated protective factors.
View Article and Find Full Text PDFJ Exerc Rehabil
December 2024
Department of Human Health Care, Gyeongsang National University, Jinju, Korea.
Aging is associated with declines in memory function and significant change in gut microbiota. In this study, we investigated how exercise affects age-related memory decline and inflammation, and gut microbiota diversity. Bl6 mice were divided into control, control and exercise, old, and old and exercise groups.
View Article and Find Full Text PDFJ Cancer
January 2025
Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, 33302, Taiwan.
Previous studies revealed that tumor-associated macrophages/microglia (TAMs) promoted glioma invasiveness during tumor progression and after radiotherapy. However, the communication of TAMs with tumor cells remains unclear. This study aimed to examine the role of small extracellular vesicles (sEVs) derived from TAMs in TAMs-mediated brain tumor invasion.
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