Background: Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the brain. Despite existing treatments, there remains an unmet need for therapies that can halt or reverse disease progression. Gene therapy has been tried and tested for a variety of illnesses, including PD. The goal of this systematic review is to assess gene therapy techniques' safety and effectiveness in PD clinical trials.
Methods: Online databases PubMed/Medline, and Cochrane were used to screen the studies for this systematic review. The risk of bias of the included studies was assessed using standard tools.
Results: Gene therapy can repair damaged dopaminergic neurons from the illness or deal with circuit anomalies in the basal ganglia connected to Parkinson's disease symptoms. Rather than only treating symptoms, this neuroprotective approach alters the illness itself. Medication for gene therapy is currently administered at the patient's bedside. It can hyperactivate specific brain circuits associated with motor dysfunction. PD therapies are developing quickly, and there aren't enough head-to-head trials evaluating the safety and effectiveness of available treatments. When choosing an advanced therapy, patient-specific factors should be considered in addition to the effectiveness and safety of each treatment option.
Conclusion: In comparison to conventional therapies, gene therapy may be advantageous for PD. It may minimize side effects, relieve symptoms, and offer dependable dopamine replacement.
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http://dx.doi.org/10.1016/j.disamonth.2024.101754 | DOI Listing |
Am J Cancer Res
December 2024
School of Basic Medical Sciences, Jiamusi University No. 258, Xuefu Street, Xiangyang District, Jiamusi 154007, Heilongjiang, China.
Breast cancer is the most common malignant tumour in women, with more than 685,000 women dying of breast cancer each year. The heterogeneity of breast cancer complicates both treatment and diagnosis. Traditional methods based on histopathology and hormone receptor status are now no longer sufficient.
View Article and Find Full Text PDFAm J Cancer Res
December 2024
Department of Hematology, Yantai Yuhuangding Hospital Yantai 264001, Shandong, China.
This review discusses multiple aspects of follicular lymphoma (FL), including etiology, treatment challenges, and future perspectives. First, we delve into the etiology of FL, which involves a variety of pathogenic mechanisms such as gene mutations, chromosomal abnormalities, immune escape, immune system dysregulation, familial inheritance, and environmental factors. These mechanisms provide the context for understanding the diversity and complexity of FL.
View Article and Find Full Text PDFUnlabelled: Quantitative understanding of mitochondrial heterogeneity is necessary for elucidating the precise role of these multifaceted organelles in tumor cell development. We demonstrate an early mechanistic role of mitochondria in initiating neoplasticity by performing quantitative analyses of structure-function of single mitochondrial components coupled with single cell transcriptomics. We demonstrate that the large Hyperfused-Mitochondrial-Networks (HMNs) of keratinocytes promptly get converted to the heterogenous Small-Mitochondrial-Networks (SMNs) as the stem cell enriching dose of the model carcinogen, TCDD, depolarizes mitochondria.
View Article and Find Full Text PDFThe maintenance of a healthy epithelial-endothelial juxtaposition requires cross-talk within glomerular cellular niches. We sought to understand the spatially-anchored regulation and transition of endothelial and mesangial cells from health to injury in DKD. From 74 human kidney samples, an integrated multi-omics approach was leveraged to identify cellular niches, cell-cell communication, cell injury trajectories, and regulatory transcription factor (TF) networks in glomerular capillary endothelial (EC-GC) and mesangial cells.
View Article and Find Full Text PDFAcute myeloid leukemias (AMLs) have an overall poor prognosis with many high-risk cases co-opting stem cell gene regulatory programs, yet the mechanisms through which this occurs remain poorly understood. Increased expression of the stem cell transcription factor, MECOM, underlies one key driver mechanism in largely incurable AMLs. How MECOM results in such aggressive AML phenotypes remains unknown.
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