Creutzfeldt-Jakob Disease (CJD) is a neurodegenerative disease characterized by mutant PrP prion proteins, which accumulates and impairs the function of wild-type PrPc proteins. The interaction of prion proteins with wild-type proteins converts the PrPc proteins to mutant PrP proteins. These mutant prion proteins lead to neural tissue degradation and other nervous system problems that can eventually lead to death. The use of antibodies to target and destroy prion proteins can be used to decrease PrP levels that can stop CJD progression. The binding affinities of different anti-PrP Fab antibodies are analyzed to determine which antibody best binds to PrP proteins and targets them for destruction. Through antibody-based targeting of prion proteins, potential treatment methods could be developed for CJD. In addition, the use of drugs, such as quinacrine and doxycycline, also show short-term effects in decreasing the progression of CJD. These drugs extend the average lifespan of tested subjects with CJD but also lead to the development of drug-resistant prion proteins that eventually cause the death of the subject affected by CJD.

DNA Double-Stranded Breaks (DSBs) are caused by genotoxic agents, such as ionizing radiation and chemical agents, and can cause an affected cell to undergo apoptosis or cell death. The process of microhomology-mediated end joining (MMEJ) shows promising results in the repair of DSBs in DNA. MMEJ is a mutagenic DSB repair mechanism that uses a certain length of homologous nucleotides adjacent to the DSB to align the broken DNA strands for repair. This can result in insertions, deletions, and even translocations of genes at the DSB site. This has led to discussions of debate on whether MMEJ is efficient in repairing DSBs in DNA. Based on the length of microhomology, the effectiveness of the DSB repair can vary. The purpose of this research is to examine MMEJ repair using micro-homologies of different lengths in Saccharomyces cerevisiae cells to test the effectiveness of MMEJ repair. The HIS3 gene located in chromosome 15 in the yeast cell is used to test for MMEJ repair, and the full microhomology length represents 311 base pairs (bp). Various crosses are performed on cells to attain desired genotypes that have the homologous chromosomes in alignment for MMEJ repair. After inducing DSBs, media-based testing is used for testing the efficiency of MMEj repair by checking for the presence of certain genes that may have formed or been deleted during the repair process.

Many children with Autism-Spectrum Disorders (ASD) struggle with sleep dysfunction. This can be caused by a lack of important gut microbiota (GM) that have the ability to influence functions of the nervous system through the gut-brain axis. The metabolites of GM function are responsible for influencing the production of pertinent sleep hormones, such as melatonin and serotonin. The research has identified lower abundance levels of the gut microbiota species Faecalibacterium and Agathobacter in children with ASD that struggled with sleep disorders. When exploring their impact on sleep hormone production, a positive correlation was identified between these species of GM and melatonin levels, which regulates circadian sleep cycles. In addition, a negative correlation was observed between these species of GM and serotonin levels, which high levels of can lead to wakefulness and sleep dysfunction. To improve GM levels in children with ASD, a Bimuno® galactooligosaccharide (B-GOS®) prebiotic intervention was tested in children with ASD. While this intervention led to improved GM levels and increased levels of Faecalibacterium growth, a significant difference was not noticed between groups. Furthermore, an analysis of probiotic intervention studies in various individuals revealed the ability to improve sleep metric scores through consumption of probiotics. These findings can be further explored in children with ASD for potential treatments for sleep disorders.