Alzheimer's disease is one of the leading causes of death in the United States and is characterized by neurodegeneration. Mishra et al. wanted to understand the role of two transport proteins, LRP1 and AQP4, in the neurodegeneration of Alzheimer's disease. They used a model organism for Alzheimer's disease, the nematode C. elegans, and genetic engineering to look at whether they would see a decrease in neurodegeneration if they increased the amount of these two transport proteins. They found that the best improvements were caused by increased expression of both transport proteins, with smaller improvements when just one of the proteins is overly expressed. Their work has important implications for how we understand neurodegeneration in Alzheimer's disease and what we can do to slow or prevent the progression of the disease.

The consumption of sugar substitute non-nutritive sweeteners (NNS) has dramatically increased in recent years. Despite being advertised as a healthy alternative, NNS have been linked to adverse effects on the body, such as neurodegenerative diseases (NDs). In NDs, neural stem cell function is impaired, which inhibits neuron regeneration. The purpose of this study was to determine if the NNS acesulfame potassium (Ace-K) and neotame affect planaria neuron regeneration rates. Since human neurons may regenerate, planaria, organisms with extensive regenerative capabilities due to stem cells called neoblasts, were used as the model organism. The heads of planaria exposed to either a control or non-toxic concentrations of NNS were amputated. The posterior regions of the planaria were observed every 24 hours to see the following regeneration stages: (1) wound healing, (2) blastema development, (3) growth, and (4) differentiation. The authors hypothesized that exposure to the NNS would slow planaria regeneration rates. The time it took for the planaria in the Ace-K group and the neotame group to reach the second, third, and fourth regeneration stage was significantly greater than that of the control. The results of this study indicated that exposure to the NNS significantly slowed regeneration rates in planaria. This suggests that the NNS may adversely impact neoblast proliferation rates in planaria, implying that it could impair neural stem cell proliferation in humans, which plays a role in NDs. This study may provide insight into the connection between NNS, human neuron regeneration, and NDs.

In this study, a deep learning model is used to classify post-traumatic stress disorder patients through novel markers to assist in finding candidate biomarkers for the disorder.

Chronic alcohol consumption can cause cardiac myopathy, which afflicts about 500,000 Americans annually. Gunturi et al. wanted to understand the effects of alcohol on heart rate and confirm the role of nitric oxide (NO) signaling in heart rate regulation. Using the model organism Daphnia magna, a water crustacean with a large, transparent heart, they found that the heart rate of Daphnia magna was reduced after treatment with alcohol. This depression could be reversed after treatment with inhibitors of NO synthesis and signaling. Their work has important implications for how we understand alcohol-induced effects on heart rate and potential treatments to reverse heart rate depression as a result of alcohol consumption.

Acquired immunodeficiency syndrome (AIDS) is a life-threatening condition caused by the human immunodeficiency virus (HIV). In this work, Takemaru et al explored the role of Coiled-Coil Domain-Containing 11 (CCDC11) in HIV-1 budding. Their results suggest that CCDC11 is critical for efficient HIV-1 budding, potentially indicating CCDC11 a viable target for antiviral therapeutics without major side effects.

Free radical chain reactions result when atoms containing unpaired electrons bind with biomolecules and alter their biological functions, contributing to the progression of diseases such as atherosclerosis, cancer, and diabetes. Antioxidants, such as vitamin E and sulforaphane, are effective neutralizers of free radicals and prevent cellular damage. This present study is conducted to determine the relative effectiveness of sulforaphane against free radicals generated by hydrogen peroxide (H2O2) compared with the known antioxidant vitamin E.

This article investigates differences in gene expression in the brains of patients with and without Parkinson's disease. The authors identify a crucial transcriptional regulator may be a relevant target for future therapeutic treatment for Parkinson's disease.

Cellular senescence plays a key role in aging cells and is attributed to a number of disease and pathology. These authors find that genetic editing of both RPS6KB1 and PPARGC1A revitalizes a human skin fibroblast cell line.

Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer, with early diagnosis and treatment challenges. When any of the genes KRAS, SMAD4, TP53, and BRCA2 are heavily mutated, they correlate with PDAC progression. Cellular stress, partly regulated by the gene SERPINA6, also correlates with PDAC progression. When SERPINA6 is highly expressed, corticosteroid-binding globulin inhibits the effect of the stress hormone cortisol. In this study, the authors explored whether there is an inverse correlation between the expression of SERPINA6 and PDAC-linked genes.

With disruption of DNA repair pathways pertinent to the timeline of cancer, thorough evaluation of mutations relevant to DNA repair proteins is crucial within cancer research. One such mutation includes S815L PMS2 - a mutation that results in significant decrease of DNA repair function by PMS2 protein. While mutation of PMS2 is associated with significantly increased colorectal and endometrial cancer risk, much work is left to do to establish the functional effects of the S815L PMS2 mutation in ovarian cancer progression. In this article, researchers contribute to this essential area of research by uncovering the tumor-progressive effects of the S815L PMS2 mutation in the context of ovarian cancer cell lines.