Researchers at the Gladstone Institute of Neurological Disease (GIND) have found a link that to a molecule that helps in understanding how Alzheimer's disease affects the brain.

The findings of the study could lead to devising specific therapeutic interventions directed to the region of the brain where the disease originates as opposed to targeting multiple brain areas.

The study pointed out to the role of amyloid β proteins that play a pivotal role in the onset and progression of Alzheimer's disease. Atypical accumulation of the protein causes the development of protein aggregates that are noxious to neurons. This build up characterizes the onset of Alzheimer's disease.

The primary brain region where Alzheimer’s disease affects is the entorhinal cortex (EC). The network between the EC and the hippocampus are vital for memory. An interruption to this network is one of the reasons of memory impairment, significant in the primary stages of the disease.

“It is not clear how EC dysfunction contributes to cognitive decline in Alzheimer's disease or whether early vulnerability of the EC initiates the spread of dysfunction through interconnected neural networks,” says Lennart Mucke, MD. “To address these questions, we studied transgenic mice with mutant APP expressed primarily in neurons of the EC.”

“Our findings directly support the hypothesis that Alzheimer's disease-related dysfunction is propagated through networks of neurons, with the EC as an important hub region of early vulnerability,” concluded Dr. Julie Harris, the lead author of the study. “Although additional studies are needed to better understand how events in the EC are related to Alzheimer's disease, it is conceivable that early interference in the EC might be of therapeutic benefit, perhaps halting disease progression.”