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.

In this study, the authors determined whether tautomerization dynamics in protic and aprotic solvents displayed differences in reaction rates and in the proportion of the keto and enol tautomers present.

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.

Caenorhabditis elegans xpa-1 and him-1 are orthologs of human XPA and human SMC1A, respectively. Mutations in the XPA are correlated with Xeroderma pigmentosum, a condition that induces hypersensitivity to ultraviolet (UV) radiation. Alternatively, SMC1A mutations may lead to Cornelia de Lange Syndrome, a multi-organ disorder that makes patients more sensitive to UVinduced DNA damage. Both C. elegans genes have been found to be involved in protection against UV radiation, but their combined effects have not been tested when they are both knocked down. The authors hypothesized that because these genes are involved in separate pathways, the simultaneous knockdown of both of these genes using RNA interference (RNAi) in C. elegans will cause them to become more sensitive to UV radiation than either of them knocked down individually. UV protection was measured via the percent survival of C. elegans post 365 nm and 5.4x10-19 joules of UV radiation. The double xpa-1/him-1 RNAi knockdown showed a significantly reduced percent survival after 15 and 30 minutes of UV radiation relative to wild-type and xpa-1 and him-1 single knockdowns. These measurements were consistent with their hypothesis and demonstrated that xpa-1 and him-1 genes play distinct roles in resistance against UV stress in C. elegans. This result raises the possibility that the xpa-1/him-1 double knockdown could be useful as an animal model for studying the human disease Xeroderma pigmentosum and Cornelia de Lange Syndrome.