Glioblastoma multiforme (GBM), a WHO grade 4 glioma, is the most common and aggressive primary brain tumor, characterized by rapid progression and poor prognosis. The heterogeneity of GBM complicates diagnosis and treatment, driving research into molecular biomarkers that can offer insights into tumor behavior and guide personalized therapies. This review explores recent advances in molecular biomarkers, highlighting their potential to improve diagnosis and treatment outcomes in GBM patients. Key biomarkers such as MGMT promoter methylation, IDH1/2 mutations, EGFR amplification, and TERT promoter mutations, etc., are examined for their roles in prognosis, therapeutic response, and tumor classification. While molecular biomarkers offer valuable insights for tailoring GBM treatments, their clinical application is hindered by tumor heterogeneity, dynamic genetic evolution, and the lack of standardized testing methods. Future research should aim to confirm new biomarkers and incorporate them into regular clinical practice to improve prognosis and treatment choices. Advances in genomic and proteomic technologies, along with consistent biomarker detection, could transform GBM care and enhance patient outcomes.

According to the WHO 2016 classification, glioblastoma is the most prevalent primary tumor in the adult central nervous system (CNS) and is categorized as grade IV. With an average lifespan of about 15 months from diagnosis, glioblastoma has a poor prognosis and presents a significant treatment challenge. Aberrant angiogenesis, which promotes tumor neovascularization and is a prospective target for molecular target treatment, is one of its unique and aggressive characteristics. Recently, the existence of glioma stem cells (GSCs) within the tumor, which are tolerant to chemotherapy and radiation, has been linked to the highly aggressive form of glioblastoma. Anti-angiogenic medications have not significantly improved overall survival (OS), despite various preclinical investigations and clinical trials demonstrating encouraging results. This suggests the need to discover new treatment options. Glioblastoma is one of the numerous cancers for which metformin, an anti-hyperglycemic medication belonging to the Biguanides family, is used as first-line therapy for type 2 diabetes mellitus (T2DM), and it has shown both in vitro and in vivo anti-tumoral activity. Based on these findings, the medication has been repurposed, which has shown the inhibition of many oncopromoter mechanisms and, as a result, identified the molecular pathways involved. Metformin inhibits cancer cell growth by blocking the LKB1/AMPK/mTOR/S6K1 pathway, leading to selective cell death in GSCs and inhibiting the proliferation of CD133+ cells. It has minimal impact on differentiated glioblastoma cells and normal human stem cells. The systematic retrieval of information was performed on PubMed. A total of 106 articles were found in a search on metformin for glioblastoma. Out of these six articles were Meta-analyses, Randomized Controlled Trials, clinical trials, and Systematic Reviews. The rest were Literature review articles. These articles were from the years 2011 to 2024. Appropriate studies were isolated, and important information from each of them was understood and entered into a database from which the information was used in this article. The clinical trials on metformin use in the treatment of glioblastoma were searched on clinicaltrials.gov. In this article, we examine and evaluate metformin’s possible anti-tumoral effects on glioblastoma, determining whether or not it may appropriately function as an anti-angiogenic substance and be safely added to the treatment and management of glioblastoma patients.

Background: Alzheimer’s disease (AD) is the most prevalent kind of dementia and is a long-term degenerative disease. Pathologically, it is defined by the development of extracellular amyloid-β plaques and intracellular neurofibrillary tangles made up of hyperphosphorylated tau protein. This causes neuronal death, particularly in the hippocampus and cortex. Mesenchymal stem cell (MSC)-derived exosomes have been identified as possibly therapeutic and have promise for Alzheimer’s disease due to their regenerative characteristics. Methods: A systematic retrieval of information was performed on PubMed. A total of 60 articles were found in a search on mesenchymal stem cells, exosomes, and Alzheimer’s disease. A total of 16 ongoing clinical trials were searched and added from clinicaltrials.gov. We added 23 supporting articles to help provide information for certain sections. In total, we included 99 articles in this manuscript: 50 are review articles, 13 are preclinical studies, 16 are clinical studies, 16 are ongoing clinical trials, and 4 are observational studies. Appropriate studies were isolated, and important information from each of them was understood and entered into a database from which the information was used in this article. The clinical trials on mesenchymal stem cell exosomes for Alzheimer’s disease were searched on clinicaltrials.gov. Results: Several experimental investigations have shown that MSC-Exo improves cognitive impairment in rats. In this review paper, we summarized existing understanding regarding the molecular and cellular pathways behind MSC-Exo-based cognitive function restoration, with a focus on MSC-Exo’s therapeutic potential in the treatment of Alzheimer’s disease. Conclusion: AD is a significant health issue in our culture and is linked to several important neuropathological characteristics. Exosomes generated from stem cells, such as mesenchymal stem cells (MSCs) or neural stem cells (NSCs), have been examined more and more in a variety of AD models, indicating that they may be viable therapeutic agents for the treatment of diverse disorders. Exosome yields may be increased, and their therapeutic efficacy can be improved using a range of tailored techniques and culture conditions. It is necessary to provide standardized guidelines for exosome manufacture to carry out excellent preclinical and clinical research.

Traumatic brain injury (TBI) is one of the leading causes of death and disability among children and adults in America. In addition, the acute morbidity caused by TBI is implicated in the development of devastating neuropsychiatric and neurodegenerative sequela. TBI is associated with the development of a neurodegenerative condition termed ‘Punch Drunk syndrome’ or ‘dementia pugilistica’, and the more recently renamed ‘chronic traumatic encephalopathy’. Chronic traumatic encephalopathy (CTE) is a slowly progressive neurodegenerative condition caused by a single or repetitive blow to the head. CTE was first described in boxers and was later found to be associated with other contact sports and military combat. It is defined by a constellation of symptoms consisting of mood disorders, cognitive impairment, and memory loss with or without sensorimotor changes. It is also a Tauopathy characterized by the deposition of hyperphosphorylated Tau protein in the form of neurofibrillary tangles, astrocytoma tangles, and abnormal neurites found in clusters around small vessels, typically at the sulcal depths. Oxidative stress, neuroinflammation, and glutaminergic toxicity caused due to the insult play a role in developing this pathology. Additionally, the changes in the brain due to aging also plays an important role in the development of this condition. In this review, we discuss the molecular mechanisms behind the development of CTE, as well as genetic and environmental influences on its pathophysiology.

One of the most prevalent primary malignant brain tumors is glioblastoma (GB). About 6 incidents per 100,000 people are reported annually. Most frequently, these tumors are linked to a poor prognosis and poor quality of life. There has been little advancement in the treatment of GB. In recent years, some innovative medicines have been tested for the treatment of newly diagnosed cases of GB and recurrent cases of GB. Surgery, radiotherapy, and alkylating chemotherapy are all common treatments for GB. A few of the potential alternatives include immunotherapy, tumor-treating fields (TTFs), and medications that target specific cellular receptors. To provide new multimodal therapies that focus on the molecular pathways implicated in tumor initiation and progression in GB, novel medications, delivery technologies, and immunotherapy approaches are being researched. Of these, oncolytic viruses (OVs) are among the most recent. Coupling OVs with certain modern treatment approaches may have significant benefits for GB patients. Here, we discuss several OVs and how they work in conjunction with other therapies, as well as virotherapy for GB. The study was based on the PRISMA guidelines. Systematic retrieval of information was performed on PubMed. A total of 307 articles were found in a search on oncolytic viral therapies for glioblastoma. Out of these 83 articles were meta-analyses, randomized controlled trials, reviews, and systematic reviews. A total of 42 articles were from the years 2018 to 2023. Appropriate studies were isolated, and important information from each of them was understood and entered into a database from which the information was used in this article. One of the most prevalent malignant brain tumors is still GB. Significant promise and opportunity exist for oncolytic viruses in the treatment of GB and in boosting immune response. Making the most of OVs in the treatment of GB requires careful consideration and evaluation of a number of its application factors.

Huntington’s disease (HD) is an inherited neurodegenerative disease characterized by uncontrolled movements, emotional disturbances, and progressive cognitive impairment. It is estimated to affect 4.3 to 10.6 per 100,000 people worldwide, and the mean prevalence rate among all published studies, reviews, and genetic HD registries is 5.7 per 100,000. A key feature of HD is the loss of striatal neurons and cortical atrophy. Although there is no cure at present, the discovery of the gene causing HD has brought us into a new DNA era and therapeutic advances for several neurological disorders. PubMed was systematically searched using three search strings: ‘“Huntington disease” + “stem cell”’, ‘”Huntington disease” + Mesenchymal stromal cell’, and ‘”Huntington disease” + “induced pluripotent stem cell”’. For each string, the search results were categorized based on cell type, and papers that included a clinical analysis were categorized as well. The data were extracted up to 2024. We did not include other databases in our search to have a comparable and systematic review of the literature on the topic. The collected data were analyzed and used for critical interpretation in the present review. Data are presented chronologically as clinical studies were published. Therapeutic strategies based on stem cells have drawn a lot of interest as possible HD therapies. Recent research indicates that NSCs have been the most often utilized stem cell type for treating HD. NSCs have been generated and extracted from a variety of sources, including HD patients’ somatic cells and the brain itself. There is strong evidence supporting the transplantation of stem cells or their derivatives in HD animal models, even if stem-cell-based preclinical and clinical trials are still in their early stages. Current treatment only aims at relieving the symptoms rather than treating the pathogenesis of the disease. Although preclinical trials in HD models have shown promise in improving cognitive and motor functions, stem cell therapy still faces many challenges and disadvantages including immunosuppression and immunorejection as well as ethical, technical, and safety concerns. Further research is required for a definitive conclusion.