Results presented at Neuroscience 2014, the annual meeting of the Society for Neuroscience (15–19 November 2014; Washington, DC), highlighted the central role of tau protein in neurodegeneration associated with Alzheimer's disease and with traumatic brain injury (TBI). Almost 36 million people worldwide suffer from Alzheimer's disease, and 10 million or more sustain TBI each year. Clarifying how tau participates in neurodegeneration may enable medical researchers to formulate strategies to halt or even reverse the damage, improving the quality of life and prognosis for those affected by these conditions.

When functioning properly, tau facilitates neurogenesis and neural activity, but dysfunctional tau can trigger neuronal apoptosis, resulting in memory loss and other neurological symptoms. Now, Julia Gerson (University of Texas Medical Branch, Galveston) and colleagues report that a specific form of tau is over-represented in the brain in both Alzheimer's disease and TBI: small aggregates of tau molecules, called tau oligomers. “Our findings add to the growing evidence that tau oligomers—not tau protein in general—are responsible for the development of neurodegenerative diseases such as Alzheimer's and for damage associated with traumatic brain injury,” Gerson explained in a press release.

Tau oligomers formed in the brain in response to TBI in rats and mice, and these oligomers closely resembled those observed in Alzheimer's disease. When injected into the brains of mice overexpressing human tau protein, the tau oligomers accelerated the onset of cognitive defects.

“Tau oligomers are likely the most toxic species of tau in neurodegenerative disease, and these results suggest that they play an important role in the toxicity underlying TBI as well. Together, these findings suggest that tau oligomers may be a viable therapeutic target in TBI and in preventing the increased acquisition of neurodegenerative disease,” concluded Gerson and her collaborators.

Another group of researchers, led by Tong Li (Johns Hopkins University, Baltimore, MD), approached the tau question from another angle, generating a new mouse model of Alzheimer's disease that expresses a mutant form of tau protein. The genetically engineered mice develop neurological symptoms similar to those observed in Alzheimer's disease, including progressive neuronal loss and memory deficits. “The new mouse model will help researchers clarify the mechanisms causing the loss of nerve cells in Alzheimer's disease,” said Li in a press release. “It will also help researchers more effectively screen new drugs for treating Alzheimer's before testing those drugs in clinical trials,” he added.