For decades the amyloid hypothesis has dominated the research field in Alzheimer’s disease. The theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques, toxic clusters of damaged proteins between cells, which eventually result in neurodegeneration. Scientists at Lund University, Sweden, have now presented a study that turns this premise on its head. The research group’s data offers an opposite hypothesis, suggesting that it is in fact the neurons’ inability to secrete beta-amyloid that is at the heart of pathogenesis in Alzheimer’s disease. Read the report of their work in Journal of Neuroscience.
adaptive immunity Alzheimer's Disease antibiotics antibodies apoptosis autism bacteria Breast cancer C. elegans cancer chromatin circadian clocks CRISPR cryo-electron microscopy DNA Drosophila Epigenetics eukaryotes evolution gene expression Genomics HIV HIV AIDS human genome immunity metabolism microRNA miRNA mitochondria mRNA neural circuits neurodegeneration neurons obesity optogenetics Parkinson's Disease pathogenesis pathogens proteomics ribosomes RNA stem cells synapses transcription vaccines