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Parkinson's disease (PD) is a prevalent and intricate neurological condition resulting from a combination of several factors, such as genetics, environment, and the natural process of aging. Degeneration of neurons in the substantia nigra pars compacta (SN) can cause motor and non-motor impairments in patients with PD. In PD's etiology, inflammation and mitochondrial dysfunction play significant roles in the disease's development. Studies of individuals with PD have revealed increased inflammation in various brain areas. Furthermore, mitochondrial dysfunction is an essential part of PD pathophysiology. Defects in the components of the mitochondrial nucleus, its membrane or internal signaling pathways, mitochondrial homeostasis, and morphological alterations in peripheral cells have been extensively documented in PD patients. According to these studies, neuroinflammation and mitochondrial dysfunction are closely connected as pathogenic conditions in neurodegenerative diseases like PD. Given the mitochondria's role in cellular homeostasis maintenance in response to membrane structural flaws or mutations in mitochondrial DNA, their dynamic nature may present therapeutic prospects in this area. Recent research investigates mitochondrial transplantation as a potential treatment for Parkinson's disease in damaged neurons. This review delves into the impact of inflammation and mitochondrial dysfunction on PD occurrence, treatment approaches, and the latest developments in mitochondrial transplantation, highlighting the potential consequences of these discoveries.

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Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) in the brain and progressive loss of dopaminergic neurons in the substantia nigra (SN) region of the brain. Although the role of neuroinflammation and cellular immunity in PD has been extensively studied, the involvement of humoral immunity mediated by antibodies and B cells has received less attention. This article provides a comprehensive review of the current understanding of humoral immunity in PD. Here, we discuss alterations in B cells in PD, including changes in their number and phenotype. Evidence mostly indicates a decrease in the quantity of B cells in PD, accompanied by a shift in the population from naïve to memory cells. Furthermore, the existence of autoantibodies that target several antigens in PD has been investigated (i.e., anti-α-syn autoantibodies, anti-glial-derived antigen antibodies, anti-Tau antibodies, antineuromelanin antibodies, and antibodies against the renin-angiotensin system). Several autoantibodies are generated in PD, which may either provide protection or have harmful effects on disease progression. Furthermore, we have reviewed studies focusing on the utilization of antibodies as a potential treatment for PD, both in animal and clinical trials. This review sheds light on the intricate interplay between antibodies and the pathological processes in PD, including complement system activation.

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BACKGROUND: Retinal degenerative disorders (RDDs) cause vision loss by damaging retinal neurons and photoreceptors, affecting individuals of all ages. Cell-based therapy has emerged as an effective approach for the treatment of RDDs with promising results. This meta-analysis aims to comprehensively evaluate the efficacy of cell therapy in treating age-related macular degeneration (AMD), retinitis pigmentosa (RP), and Stargardt macular degeneration (SMD) as the most prevalent RDDs. METHODS: PubMed, Scopus, Web of Science, and Embase were searched using keywords related to various retinal diseases and cell therapy treatments until November 25th, 2023. The studies' quality was evaluated using the Joanna Briggs Institute's (JBI) checklist for quasi-experimental studies. Visual acuity measured as LogMAR score was used as our main outcome. A three-level random-effect meta-analysis was used to explore the visual acuity in patients who received cell-based therapy. Heterogeneity among the included studies was evaluated using subgroup and sensitivity analyses. Moreover, meta-regression for the type of cells, year of publication, and mean age of participants were performed. RESULTS: Overall, 8345 studies were retrieved by the search, and 39 met the eligibility criteria, out of which 18 studies with a total of 224 eyes were included in the meta-analysis. There were 12 studies conducted on AMD, 7 on SMD, and 2 on RP. Cell therapy for AMD showed significant improvement in LogMAR (p < 0.05). Also, cell therapy decreased the LogMAR score in SMD and RP (p < 0.01 and p < 0.0001, respectively). Across all conditions, no substantial publication bias was detected (p < 0.05). CONCLUSION: The findings of the study highlight that the application of cell therapy can enhance the visual acuity in AMD, SMD, and RP.

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BACKGROUND: Breast cancer is the leading cause of cancer worldwide. The high expenses associated with chemotherapy as well as its side effects make the management of breast cancer a daunting challenge. The most common overexpressed gene in breast cancer is cyclinD1, which induces cell proliferation. Recent investigations into cancer treatment have revealed that curcumin demonstrates potential anti-cancer properties through different pathways. However, the oral bioavailability of curcumin is negligible due to its high hydrophobic structure. Nanotechnology has been employed to overcome this barrier. Nano-formulated curcumin (SinaCurcumin®) has been shown to provide a significantly higher bioavailability for oral consumption. However, the efficacy of this nano-formulated drug in breast cancer has not yet been determined. In relation to the breast cancer cell line, the present study compared nano-curcumin's anti-cancer properties with those of cyclophosphamide, adriamycin, and 5-fluorouracil (CAF). METHODS: After treating MCF7 with nano-curcumin and CAF, the present work assessed cell viability via an MTT assay. The effects of these drugs on cyclinD1 expression were measured by real-time PCR. SPSS 16.0 was used to perform ANOVA and multiple range tests. RESULTS: Nano-curcumin and the CAF regimen both lowered the viability of MCF7. Nano-curcumin decreased cell proliferation by 83.6%, which was more than that achieved by cyclophosphamide (63.31%), adriamycin (70.75%), and 5-fluorouracil (75.04%). In addition, curcumin was able to significantly reduce the expression of cyclinD1, whereas CAF did not alter cyclinD1 expression. CONCLUSION: Nano-curcumin has a relatively high cytotoxic effect on MCF7 breast cancer cells, suppressing the expression of cyclinD1, a critical gene in the development and metastasis of breast cancer. The current study demonstrated that nano-curcumin can be an effective drug in the CAF regimen for the treatment of breast cancer. However, further in vivo research is needed for determining its efficacy and safety in clinical applications.