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Alzheimer’s disease (AD) is a type of dementia that affects more than 5.5 million Americans, and there are no approved treatments that can delay the advancement of the disease. In this work, Xu and Mitchell test the effects of various herbal extracts (bugleweed, hops, sassafras, and white camphor) on Aβ_1-40 peptide levels in human neuroblastoma cells. Their results suggest that bugleweed may have the potential to reduce Aβ_1-40 levels through its anti-inflammatory properties.

Oxidative damage and neuro-inflammation were the key pathways implicated in the pathogenesis of Alzheimer’s disease. In this study, 30 natural extracts from plant roots and leaves with extensive anti-inflammatory and anti-oxidative properties were consumed by Drosophila melanogaster. Several assays were performed to evaluate the efficacy of these combinational extracts on delaying the progression of Alzheimer’s disease. The experimental group showed increased motor activity, improved associative memory, and decreased lifespan decline relative to the control group.

Enzyme chemotaxis is a thermodynamic phenomenon in which enzymes move along a substrate concentration gradient towards regions with higher substrate concentrations and can be used to steer nanovehicles towards targets along natural substrate concentrations. In patients with Alzheimer’s disease, a gradient of tau protein forms in the bloodstream. Tau protein is a substrate of the enzyme CDK5, which catalyzes the phosphorylation of tau protein and can travel using chemotaxis along tau protein gradients to increasing concentrations of tau and amyloid-beta proteins. The authors hypothesized that CDK5 would be able to overcome these barriers of Brownian motion and developed a quantitative model using Michaelis-Menten kinetics to define the necessary parameters to confirm and characterize CDK5’s chemotactic behavior to establish its utility in drug delivery and other applications.

Alzheimer’s disease (AD) is a common disease affecting 6 million people in the U.S., but no cure exists. To create therapy for AD, it is critical to detect amyloid-β protein in the brain at the early stage of AD because the accumulation of amyloid-β over 20 years is believed to cause memory impairment. However, it is difficult to examine amyloid-β in patients’ brains. In this study, we hypothesized that we could accurately predict the presence of amyloid-β using EEG data and machine learning.

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.

Here, the authors investigated the role of nonpharmacological interventions in preventing or delaying cognitive impairment in individuals with and without dementia. By using a retrospective case-control study of 22 participants across two senior centers in San Diego, they found no significant differences in self-reported activities. However, they found that their results reflected activity rather than the activity itself, suggesting the need for an alternative type of study.

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.