Groundbreaking Study Reveals How Alzheimer’s Pathology Reshapes Daily Cellular Rhythms A revolutionary study published in Nature Neuroscience has uncovered how…
Scientists have discovered that loss of TDP-43 protein from cell nuclei triggers widespread errors in genetic processing in neurodegenerative diseases. The findings reveal how alternative polyadenylation changes contribute to frontotemporal dementia and ALS pathology through multiple disease-relevant genes.
Researchers have uncovered a crucial mechanism by which TDP-43 protein dysfunction contributes to frontotemporal dementia and amyotrophic lateral sclerosis, according to a new study published in Nature Neuroscience. The report indicates that loss of TDP-43 from neuronal nuclei causes widespread changes in alternative polyadenylation (APA), a fundamental genetic processing mechanism that determines where RNA molecules are cut and adding a tail of adenine nucleotides.
In a major genomic advancement, researchers have successfully sequenced the complete genome of the endangered Anqing Six-end-white pig at chromosome-level resolution. The study reveals comprehensive genetic insights that could revolutionize conservation and breeding programs for this unique Chinese heritage breed.
Scientists have reportedly achieved the first chromosome-level genome assembly of the Anqing Six-end-white pig, according to research published in Scientific Data. The comprehensive sequencing project, sources indicate, combined multiple advanced technologies including short reads, PacBio HiFi reads, and Hi-C sequencing data to create one of the most complete porcine genome maps to date.
