In this study, the authors observe if the symptoms of Rett Syndrome, a neurodegenerative disease in humans, are reflected in Drosophila melanogaster. This was achieved by differentiating the behavior and physical aspects of wild-type flies from flies expressing the full-length MeCP2 gene and the mutated MeCP2 gene (R106W). After conducting these experiments, some of the Rett Syndrome symptoms were recapitulated in Drosophila, and a subset of those were partially ameliorated by the introduction of pifithrin-alpha.
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.
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.
Dental resins can be a source of reactive oxygen species (ROS) which in unruly amounts can be toxic to cellular and overall health. In this report, the authors test whether the consumption of antioxidant rich foods like avocado and asparagus can protect against the effect of dental resin-derived ROS. However, rather than testing humans, they use fruit flies and their climbing abilities as an experimental readout.
The authors assess a genetic variant within a well-known interaction partner of huntingtin that has been linked to modifying the age of onset of Huntington's disease.
The authors use known Parkinson's disease-associated genetic variants to compare the prevalence of sleep dysfunction between males and females diagnosed with Parkinson's disease.
Parkinson’s disease (PD) is a prevalent neurodegenerative disorder in the U.S., second only to Alzheimer’s disease. Current diagnostic methods are often inefficient and dependent on clinical exams. This study explored using machine and deep learning to enhance PD diagnosis by analyzing spiral drawings affected by hand tremors, a common PD symptom.
Autism Spectrum Disorder (ASD) and Alzheimer's Disease (AD) are distinct conditions, but research suggests a link, as individuals with ASD are 2.5 times more likely to develop AD. A study employing genome-wide association studies and Mendelian randomization revealed shared genetic factors, particularly in synaptic regulation pathways, that may increase the risk of AD in those with ASD. These findings provide insights into the genetic underpinnings connecting the two disorders.
The degeneration of nerve cells in the brain can lead to pathologies such as Parkinson’s disease. It has been suggested that neurons in humans may regenerate. In this study, the effect of different doses of caffeine on regeneration was explored in the planeria model. Caffeine has been shown to enhance dopamine production, and dopamine is found in high concentrations in regenerating planeria tissues. Higher doses of caffeine accelerated planeria regeneration following decapitation, indicating a potential role for caffeine as a treatment to stimulate regeneration.
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.
