Researchers found that excitatory neurons — those that are more likely to trigger an action (as opposed to inhibitory neurons, which are less likely to prompt neural activity) — are more vulnerable to accumulations of abnormal tau protein, which is increasingly being implicated in Alzheimer’s disease.
Even as they’ve struggled to highlight parts of the human genome worth investigating, scientists have wondered how much they’re actually learning through the methods they use. Now, two researchers have determined that natural selection and our own evolutionary history might be science’s best critics, and guides for future research.
Researchers have genetically modified a common houseplant to remove chloroform and benzene from the air around it.
Loss of the protein Parkin causes certain forms of Parkinson’s disease, a neurodegenerative condition involving death of neurons. Scientists have now shown that Parkin stifles cell death by blocking BAK, a protein which is a central player in cell death. Understanding the interactions between Parkin and BAK may lead to new therapeutic approaches to slow the progression of Parkinson’s disease.
Researchers have discovered new changes occurring in the human brain in the early stages of Alzheimer’s disease. The researchers used a multiomic approach to determine RNA, protein, and phosphorylation levels and carried out further neurobioinformatic analyses on them.
Researchers analyzed skin cells from the very young to the very old and looked for molecular signatures that can be predictive of age. By applying machine-learning algorithms to these biomarkers, they were able to predict a person’s actual age with less than eight years error, on average.
Researchers have discovered a new use for a long-standing computational concept known as ‘blacklisting.’ Using blacklisting as a filter to single out genetic variations in patient genomes and exomes that do not cause illness, researchers have successfully streamlined the identification of genetic drivers of disease.
Incorporating genetic diversity into a mouse model of Alzheimer’s disease resulted in greater overlap with the genetic, molecular and clinical features of this pervasive human disease, according to a new study.