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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.

In this article the authors address the complex and life quality-diminishing neurodegenerative disease known as Parkinson's. Although genetic and/or environmental factors contribute to the etiology of the disease, the diagnostic symptoms are the same. By genetically modifying fruit flies to exhibit symptoms of Parkinson's disease, they investigate whether drugs that inhibit mitochondrial calcium uptake or activate the lysosomal degradation of proteins could improve the symptoms of Parkinson's these flies exhibit. The authors report the most promising outcome to be that when both types of drugs were used together. Their data provides encouraging evidence to support further investigation of the utility of such drugs in the treatment of human Parkinson's patients.

The authors looked at whether retinal features, specifically lens clarity, optic nerve cupping, and hyperreflective foci, can serve as biomarkers for neuro-ophthalmological diseases, which share pathological mechanisms with neurodegeneration and may indicate broader neurological risk. Using multimodal clinical data and machine learning, they investigated the potential of retinal imaging as a complementary diagnostic tool for more accurate and accessible detection of neurological disorders.

The authors looked at whether they could induce the formation of new neurons from astrocytes via the upregulation of a microRNA (miR-124a). They found that upregulation of miR-124a started transdifferentiation of neurons, but was not enough to lead to full conversion of astrocytes to neurons.

The authors use molecular modeling to test analogs of the stearoyl-coenzyme A desaturase 1 (SCD1) inhibitor MF-438 with implications for future development of Parkinson's disease therapeutics.

Molecules which bind to proteins that aggregate abnormally in neurodegenerative diseases could be promising drugs for these diseases. In this study, Zhang, Wu, Zhang, and Dang simulate the binding behavior of various molecules to screen for candidates which could be promising candidates for drug development.

Kalirin is a guanine nucleotide exchange factor (GEF) for the GTPase RAC1, linked to schizophrenia and Alzheimer’s Disease. It plays a crucial role in synaptic plasticity by regulating dendritic spine formation and actin cytoskeleton remodeling, which are essential for creating new synapses. Authors developed two novel compounds targeting kalirin, confirming that predictive modeling can indicate biological activity.

E-cigarettes are often considered a healthier alternative to traditional cigarettes. This team of high school authors investigated the impact of common e-cigarette compounds on C. elegans, and found a number of harmful effects ultimately resulting in injury and neuronal damage.

The authors employ computational protein design to identify a mini-protein with the potential to enhance binding of the tight junction protein, claudin-5, at the blood-blood barrier with therapeutic potential for neurodegenerative diseases.

Here the authors hypothesized that reducing folliculin (FLCN) might affect p62 protein levels in the dorsal hippocampus of mice, given their potential functional connection and p62's role in neurodegenerative diseases. Their study, using western blots and a two-way ANOVA on young wild-type mice, found that p62 levels correlated with FLCN expression, but ultimately concluded there's no evidence of a functional connection between FLCN and p62 in this specific model.