New Insights Into How Alzheimer’s and Related Diseases Spread in the Brain
WASHINGTON, DC — Studies released today reveal important new evidence about the central role that a protein called tau plays in the progression of Alzheimer’s disease, traumatic brain injury (TBI), and other disorders characterized by a steady loss of brain cells. The findings were released at Neuroscience 2014, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
Most previous research into Alzheimer’s and related diseases has focused on a protein called beta amyloid, which forms sticky plaques that are believed to strangle healthy neurons. Recently, scientists have also turned their attention to a second protein: tau. When tau is working properly in the brain, it helps with the building and functioning of neurons. When tau malfunctions, however, it creates abnormal clumps of protein fibers, known as neurofibrillary tangles, which may not only trigger cell death, but also spread rapidly throughout the brain.
Worldwide, nearly 36 million people are living with Alzheimer’s or other types of dementia, according to Alzheimer’s Disease International. The World Health Organization estimates that more than 10 million people sustain a TBI each year. Understanding tau’s connection to these brain disorders could have implications for possible future treatments.
Today’s new findings show that:
- The symptoms of both Alzheimer’s disease and TBI are associated in mice with the overproduction of the same toxic form of the tau protein (Julia Gerson, abstract 482.06, see attached summary).
- Immune cells called microglia may help trigger the spread of Alzheimer’s-associated toxic protein in rodents (Tsuneya Ikezu, MD, PhD, abstract 578.08, see summary attached).
- New mouse models containing both tau tangles and amyloid plaques may offer scientists a more accurate research tool for studying Alzheimer’s disease (Tong Li, PhD, abstract 578.04, see summary attached).
Other recent findings discussed show that:
- Injecting tau fibrils into the brain in mice models triggers the formation and spread of tau-containing structures that lead to cell death (Diederik Moechars, PhD, presentation 482.04, see attached speaker summary).
- A drug that boosts the function of a specific type of chemical receptor in the brain is able to reverse dementia-like behavior in mice with a tau mutation associated with frontotemporal dementia (Erik Roberson, MD, PhD, presentation 578.03, see attached speaker summary).
“As this research illustrates, the tau protein plays an incredibly complex role in the development of Alzheimer’s and other neurodegenerative diseases,” said Sangram Sisodia, PhD, director of the Center for Molecular Neurobiology at the University of Chicago and an expert on Alzheimer’s disease. “We are in the early stages of understanding the role of the tau protein, which will be crucial for developing effective preventions or treatments.”
This research was supported by national funding agencies such as the National Institutes of Health as well as other private and philanthropic organizations. Find out more about the tau protein and its role in Alzheimer’s and other brain diseases at BrainFacts.org.
