Anticholinergics are used in treating asthma, a chronic inflammation of the airways. These drugs block human M1 and M2 muscarinic acetylcholine receptors, inhibiting bronchoconstriction. However, studies have reported complications of anticholinergic usage, such as exacerbated eosinophil production and worsened urinary retention. Modification of known anticholinergics using bioisosteric replacements to increase efficacy could potentially minimize these complications. The present study focuses on identifying viable analogs of anticholinergics to improve binding energy to the receptors compared to current treatment options. Glycopyrrolate (G), ipratropium (IB), and tiotropium bromide (TB) were chosen as parent drugs of interest, due to the presence of common functional groups within the molecules, specifically esters and alcohols. Docking score analysis via AutoDock Vina was used to evaluate the binding energy between drug analogs and the muscarinic acetylcholine receptors. The final results suggest that G-A3, IB-A3, and TB-A1 are the most viable analogs, as binding energy was improved when compared to the parent drug. G-A4, IB-A4, IB-A5, TB-A3, and TB-A4 are also potential candidates, although there were slight regressions in binding energy to both muscarinic receptors for these analogs. By researching the effects of bioisosteric replacements of current anticholinergics, it is evident that there is a potential to provide asthmatics with more effective treatment options.

Naturally occurring neuroactive alkaloids are often studied for their potential to treat Neurological diseases. This team of students study Rivastigmine, a potent cholinesterase inhibitor that is a synthetic analog of physostigmine, which comes from the Calabar bean plant Physostigma venenosum. By comparing the effects of optimized synthetic analogs to the naturally occurring alkaloid, they determine the most favorable analog for inhibition of acetylcholinesterase (AChE), the enzyme that breaks down the neurotransmitter acetylcholine (ACh) to terminate neuronal transmission and signaling between synapses.

Alzheimer's disease (AD) involves the reduction of cholinergic activity due to a decrease in neuronal levels of nAChR α7. In this work, Sanyal and Cuellar-Ortiz explore the role of the nAChR α7 in learning and memory retention, using Drosophila melanogaster as a model organism. The performance of mutant flies (PΔEY6) was analyzed in locomotive and olfactory-memory retention tests in comparison to wild type (WT) flies and an Alzheimer's disease model Arc-42 (Aβ-42). Their results suggest that the lack of the D. melanogaster-nAChR causes learning, memory, and locomotion impairments, similar to those observed in Alzheimer's models Arc-42.

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.