Researchers at Oregon Health & Science University's Neurological Sciences Institute (NSI) have shed light on the brain cell damage caused by Alzheimer's disease.
The researchers hope that by gaining a better understanding of the disease's cellular impacts, progress can be made towards developing a treatment. The research is reported in the current edition of the Journal of Alzheimer's Disease, published by IOS publishers.
While the cognitive and behavioral impacts of Alzheimer's can be clearly witnessed in patients, the disease's cellular function and methods for disrupting thought and memory have not been well understood. By conducting this research, NSI scientists and their collaborators have demonstrated how proteins involved in brain cell communications, called synaptic proteins, decrease in the brains of Alzheimer's patients when compared to healthy brains from people in the same age range.
"More importantly, we found that the decrease of synaptic protein levels in the frontal cortex of the brains of Alzheimer's patients was more severe than in other portions of the brain," explained P. Hemachandra Reddy, Ph.D., scientist at the Neurological Sciences Institute and first and corresponding author of the paper. "Because the frontal cortex is home to important brain functions such as reasoning, planning, and abstract thought – all affected by Alzheimer's – this finding appears to be significant. Furthermore, we noticed that synaptic protein levels were even lower in the brains of patients in the early stages of Alzheimer's disease. This suggests to us that the loss of these important proteins happens very early in the disease process."
One possible reason for the reduction of synaptic proteins is mitochondrial dysfunction, a well-documented occurrence in Alzheimer's. The researchers believe it's possible that defective mitochondria in Alzheimer's neurons may not move effectively and may not supply adequate levels of Adenosine Triphosphate (ATP). ATP is an important cellular chemical that bonds at nerve terminals for normal neural communication. The low levels of cellular ATP at nerve terminals may lead to the loss of synapses and synaptic function, and may ultimately cause cognitive decline in AD patients.