Better tactics for detecting, preventing, and treating Alzheimer's disease depend on a clearer understanding of cellular-level changes in the minds of patients, and a study appearing in in the journal Nature Neuroscience has uncovered novel details about the vulnerability of one type of brain cell.
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 increasingly is being implicated in Alzheimer's disease. The study also uncovered some possible genetic explanations for the vulnerability of those cells, work that one day has the potential to lead to targeted treatment.
The study was co-led by Hongjun "Harry" Fu, assistant professor of neuroscience at Ohio State University, along with Karen Duff (professor of pathology and cell biology at Columbia University) and Michele Vendruscolo (professor in the Department of Chemistry at the University of Cambridge).
Much of the research on Alzheimer's disease in the past focused on the buildup of amyloid beta proteins in the brain, but work by Fu and his collaborators is focused on tau.
Tau plays an important role in normal, healthy neurological activity but, when it builds up within neurons early on in the progression of Alzheimer's disease, it clogs and then kills those cells. Excessive accumulation of the abnormal tau protein also has been linked to other neurological diseases, including dementia and traumatic brain injury, indicates Fu, who is a member of the Neurological Institute at OSU's Medical Center and part of the Chronic Brain Injury program.
The researchers studied the brains of patients who had Alzheimer's disease and also a mouse model and found that the abnormal tau protein accumulated predominantly in excitatory neurons, rather than inhibitory neurons.
Then, using genetic analysis from the brains of donors who did not have Alzheimer's disease or other...