Alzheimer's disease is a progressive neurodegenerative disorder, thought to be caused by buildup of proteins in the brain. But there is increasing evidence that different biological processes are at the heart of the disease, providing scientists with a different approach to possible therapies.
In a plenary session delivered at the Alzheimer's Association International Conference (AAIC) 2017, held in London, United Kingdom, Julie Williams, Ph.D. - a professor in the Division of Psychological Medicine and Clinical Neurosciences at Cardiff University in the U.K. - challenged the traditional views of Alzheimer's disease by saying that \"immunity is playing a significant role\" in the disease.
Alzheimer's disease is the sixth leading cause of death in the United States, affecting more than 5 million adults in the country.
The traditional view is that proteins accumulate in the brains of patients, leading to neuronal death. The culprits are the amyloid beta peptide and the tau protein.
Amyloid beta is produced when a short section of the amyloid precursor protein (APP) is severed. The function of the peptide in normal brain function is not known, but some evidence points toward a role in neurons. In Alzheimer's disease, amyloid beta accumulates in plaques in the spaces between neurons.
Tau is a structural protein, important for neuronal function. But in Alzheimer's, tau does not function properly and accumulates in tangles in neurons. How this contributes to cell death is unknown, but there is new evidence that shows that abnormal tau processing can lead to toxic effects.
How are scientists challenging the traditional view that abnormal protein buildup in the brain is to blame for the neurodegeneration seen in Alzheimer's disease?