Study Links Alzheimer's with Toxic Protein Fragments
New research from the Gladstone Institute of Neurological Disease details exactly how a mutant form of the protein apolipoprotein E, also known as apoE, is a causative factor for Alzheimer's disease.
It pinpoints mitochondria, the organelles within cells designed to turn glucose into energy, as a key site that specific fragments of a particular form of apoE attack, leading to the neuronal death characteristic of Alzheimer's disease (AD). The findings are published online by the Proceedings of the National Academy of Science, in advance of the Dec. 20 issue of PNAS.
According to Gladstone Assistant Investigator Yadong Huang, M.D., Ph.D., who headed the study, it has been known for several years that a correlation exists between lowered glucose metabolism and the presence in the brain of a mutant form of a protein that transports cholesterol.
Scientists have been unable to determine if this mutant protein actually interferes with the ability of neurons to make use of glucose in the brain, but they have theorized that such an inability to access glucose might kill off crucial brain cells, causing