β-Amyloid (Aβ) is a hallmark peptide of Alzheimer’s disease (AD). Herein, we explored the mechanism underlying the cytotoxicity of this peptide. Double treatment with oligomeric 42-amino-acid Aβ (Aβ42) species, which are more cytotoxic than other conformers such as monomers and fibrils, resulted in increased cytotoxicity. Under this treatment condition, an increase in intracellular localization of the peptide was observed, which indicated that the peptide administered extracellularly entered the cells. The cell-permeable peptide TAT-tagged Aβ42 (tAβ42), which was newly prepared for the study and found to be highly cell-permeable and soluble, induced Aβ-specific lamin protein cleavage, caspase-3/7-like DEVDase activation, and high cytotoxicity (5–10-fold higher than that induced by the wild-type oligomeric preparations). Oligomeric species enrichment and double treatment were not necessary for enhancing the cytotoxicity and intracellular location of the fusion peptide. Taiwaniaflavone, an inhibitor of the cytotoxicity of wild-type Aβ42 and tAβ42, strongly blocked the internalization of the peptides into the cells. These data imply a strong relationship between the cytotoxicity and intracellular location of the Aβ peptide. Based on these results, we suggest that agents that can reduce the cell permeability of Aβ42 are potential AD therapeutics.

For the study of amyloid beta (Aβ) associated toxicity which is supposed to be the main pathological agent in Alzheimer’s disease (AD), it is important to secure Aβ peptide with appropriate biological activity. However, commercial and synthetic Aβ often have some pitfalls like less cell toxicity, prompt aggregation and excess price, using recombinant technology, these issues can be resolved though the method also suffered from some problems such as low yield, aggregation and prolong time to purify. Thus, we previously developed an easy, economic and convenient method for Aβ42 purification using highly expressed GroES-Ubiquitin-Aβ42 fusion protein. The method was efficient, but further development was performed to improve the procedure and increase the yield. Focus was on the isolation of the fusion protein (GroES-Ubiquitin) from Aβ42 peptide. After a series of systematic testing with several chemicals, we found that methanol could precipitate efficiently the fusion protein, while the Aβ peptide was recovered in the supernatant. By this method, Aβ peptide was easily purified without tedious chromatographic steps which are main obstacles to purify the peptide in the previous method. This method yielded ~20 mg highly pure Aβ42 peptide from 1-liter bacterial culture. Different biophysical characterizations and bioactivity assays indicate that the peptide purified using this method was competitive with others which have been previously reported whereas considering the simplicity, final yield and time of purification, this method is the optimal solution.

Objectives: Breast cancer is one of the most common malignancies in women. The PD1 and MTNR1B gene polymorphisms have been extensively studied for their potential role in cancer susceptibility. This study aimed to investigate associations between breast cancer risk and PD1 (rs36084323) and MTNR1B (rs10830963) polymorphisms.Methods: A case–control study was conducted with 112 breast cancer patients from Dhaka Cancer and General Hospital, Bangladesh, and 124 age‐ and sex‐matched healthy controls. Genotyping of PD1 (rs36084323) and MTNR1B (rs10830963) polymorphisms was performed using the Polymerase Chain Reaction–Restriction Fragment Length Polymorphism (PCR‐RFLP) method.Results: The genotype distributions for both SNPs adhered to Hardy–Weinberg equilibrium (HWE). The PD1 GG genotype was more prevalent in controls, indicating a protective effect, whereas the GG genotype of MTNR1B showed no statistically significant association with breast cancer risk. The recessive model of PD1 (GG vs. AG + AA) demonstrated a lower odds ratio (0.2873), while the recessive model of MTNR1B (2.307) suggested a potential risk. Dominant models for both genes (AG + GG vs. AA for PD1 and CG + GG vs. CC for MTNR1B) showed statistically significant associations with breast cancer susceptibility.Conclusion: The PD1 GG genotype exhibited a significant protective effect against breast cancer, while the MTNR1B CG genotype was associated with reduced risk, but GG showed no correlation. Larger studies across diverse populations are recommended to validate these findings.

Amyloid‐β‐42 (Aβ42) internalization plays a critical role in Alzheimer's disease (AD) pathology. We investigated whether biflavonoids, natural small molecules, could inhibit Aβ42 uptake and mitigate its cytotoxicity. Biochemical and imaging analyses revealed that biflavonoids dose‐dependently blocked Aβ42 internalization, preventing lamin fragmentation and caspase activation which are considered as key steps in Aβ42‐induced cell death. Confocal microscopy and Western blotting confirmed reduced Aβ42 entry, while aggregation assays in cell‐free conditions demonstrated biflavonoids suppress Aβ42 fibril, oligomer, and β‐sheet formation. These findings suggest biflavonoids exert cytoprotective effects by inhibiting both Aβ42 conformational changes and cellular uptake, positioning them as promising anti‐amyloidogenic agents for AD therapy.

Background: Breast cancer (BC) is the most common malignancy among Bangladeshi women. MDM4 gene polymorphisms have been implicated in BC susceptibility, but data from South Asian populations remain limited. Methods: This case–control study included 112 BC patients from a cancer hospital, Dhaka, Bangladesh, and 124 age‐ and sex‐matched healthy controls (HC) from the surrounding areas. Genotyping of MDM4 rs1380576 and rs4245739 polymorphisms was performed using the polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) method. Results: Genotype distributions of both polymorphisms conformed to Hardy–Weinberg equilibrium. No association was observed for rs4245739 A>C under any genetic model. In contrast, rs1380576 C>G showed an increased BC risk for CC versus GG (aOR = 3.93; 95% CI = 2.09–7.38; p < 0.001) and for CG + CC versus GG (aOR = 2.04; 95% CI = 1.19–3.50; p = 0.009). The recessive model also indicated elevated risk for CC carriers (aOR = 4.58; 95% CI = 2.46–8.55). A protective effect was observed for the heterozygous genotype in the over‐dominant model (aOR = 0.11; 95% CI = 0.02–0.47; p = 0.003). Conclusion: The MDM4 rs1380576 C>G polymorphism, particularly the CC genotype, is associated with increased BC risk in Bangladeshi women, whereas rs4245739 A>C shows no association. These findings suggest rs1380576 may serve as a potential genetic marker for BC susceptibility in this population.

Background and Aims: The Dinga Dinga Virus (DDV) has emerged as a mysterious disease gripping women in Uganda, raising alarm due to its unusual and distressing “dancing” like symptoms. These symptoms, characterized by involuntary movements resembling dance, suggest possible neurological involvement, though the exact pathogen remains unidentified. The causative agent for DDV is still unknown. We hypothesized that the possible microorganism could be a virus, bacteria, or vector‐borne origin. Therefore, comprehensive research is urgently needed to confirm its cause. Methods: We performed a comprehensive literature search in Scopus and Web of Science related to the different outbreaks of viruses. We collected relevant information from appropriate articles for this review. Results: The unique representation of the disease is spreading rapidly in localized areas that have the potential to escalate into a broader public health crisis. Preventive measures focused on symptom monitoring, public awareness, and isolation of suspected cases to limit transmission. Authorities emphasize hygiene practices, using personal protective equipment (PPE), and early reporting to manage the outbreak effectively. Simultaneously, global health organizations are being called to collaborate on diagnostic development, therapeutic interventions, and vaccine research. The disproportionate impact on women has brought social and cultural dynamics into the spotlight, as stigma and misinformation exacerbate the outbreak's challenges. Immediate and long‐term strategies must address these aspects by strengthening healthcare infrastructure and enhancing disease surveillance systems. Conclusion: As the world recovers from the COVID‐19 pandemic, the DDV is a stark reminder of the ongoing threat of emerging infectious diseases. Proactive, science‐driven efforts are critical to understanding and mitigating this enigmatic disease, ensuring it does not escalate into another global health crisis.