New research from Georgetown University Medical Center has revealed information on Alzheimer’s disease that drastically changed many assumptions in its progression and development. The study, published in the scientific journal Molecular Neurodegeneration, has discovered that neuron death, one of the major effects of Alzheimer’s, may be influenced by tau proteins. This phenomenon was previously believed to be caused by amyloid-beta, or Abeta, plaque peptides. The results help explain why certain people with buildups of Abeta plaque do not have dementia or related disorders. It also enables experts to more accurately pinpoint possible Alzheimer’s cases among potential patients. This discovery dramatically alters the medical understanding of Alzheimer’s disease, and also reveals more key information on the factors that could cause the disorder.
Alzheimer’s disease is one of the most widespread forms of dementia that gets worse with old age. Alzheimer’s currently has no cure and ends in death for its patients. Symptoms of the disease include short and long term memory loss, impaired cognitive ability, drastic mood swings, confusion, frustration, and aggression. Many Alzheimer’s patients have difficulty in relating to other people and end up becoming socially withdrawn from their friends and family. As the disease progresses, the functions of the rest of the body slowly begin to break down and lead to death approximately seven years after an initial diagnosis are made. Alzheimer’s is a neurodegenerative disorder, wherein the neurons slowly begin to lose their structure and function, eventually leading to death.
Amyloid beta plaques
While a definitive cause behind Alzheimer’s has yet to be established, it is believed that amyloid beta peptides do play a major influencing role. Amyloid beta peptides stick together as groups of protein aggregates known as amyloid plaques. These plaques are commonly found in the brains of Alzheimer’s patients, as well as those with other kinds of dementia disorders. Many medical experts support the amyloid hypothesis, which states that these amyloid plaques are a major causal agent that contributes to the development of Alzheimer’s. They believe that accumulations of plaque produce toxic effects on neural cells and result in death.
Role of tau proteins
Doctor Charbel E-H Moussa, senior investigator of the Georgetown Medical Center study, discerned that the neuronal death associated with dementia is controlled by tau proteins instead of amyloid beta plaques. Abnormalities in tau in the brain cause amyloid proteins to accumulate as sticky plaque aggregates inside neurons. While the cells attempt to force these protein clumps out, any amyloid proteins that remain in the cell, along with any tau proteins that are not functioning, become responsible for cell death. Moussa’s research showed that fewer amounts of plaque gathered outside cells with fully functioning tau. Malfunctioning tau proteins prevent brain cells from clearing out toxic waste and lead to amyloid plaque build-up. Thus, it is important that tau proteins are able to function properly to prevent any neuron death from occurring as a result of amyloid aggregation.
A known cure or cause behind Alzheimer’s disease has yet to be established, thus the information discovered in the Georgetown study does present some promising results. Tracking the effects of malfunctioning tau in the brain can be difficult, as some proteins may appear normal while others may have already lost function. In some cases, tau defects may not cause amyloid plaques to form. Moussa’s goal is to find a way to assist functional tau in clearing up neural garbage. He has already worked on the approved cancer drug nilotinib, but claims that it still needs levels of functioning tau to work properly.