Increased Neuronal Activity Stimulates Spread of Tau Proteins in the Brain

By LabMedica International staff writers
Posted on 04 Aug 2016
Neurodegenerative disease researchers have found that tau proteins released from donor neurons can transfer to recipient cells via the medium, suggesting that at least one mechanism by which tau can transfer in the brain is via the extracellular space.

Tau proteins are proteins that stabilize microtubules. They are abundant in neurons of the central nervous system and are less common elsewhere, but are also expressed at very low levels in central nervous system astrocytes and oligodendrocytes. Pathologies and dementias of the nervous system such as Alzheimer's disease and Parkinson's disease are associated with tau proteins that have become defective and no longer stabilize microtubules properly.

Image: In this photomicrograph, the color orange indicates where tau protein has traveled from one neuron to another (Photo courtesy of Dr. Karen E. Duff, Columbia University Medical Center).

Investigators at Columbia University Medical Center (New York, NY, USA) reported in the June 20, 2016, online edition of the journal Nature Neuroscience that they had used optogenetic and chemogenetic approaches to show that increased neuronal activity stimulated the release of tau in vitro and enhanced tau pathology in vivo.

"These findings suggest that clinical trials testing treatments that increase brain activity, such as deep brain stimulation, should be monitored carefully in people with neurodegenerative diseases," said senior author Dr. Karen Duff, professor of pathology and cell biology at the Columbia University Medical Center. "By learning how tau spreads, we may be able to stop it from jumping from neuron to neuron. This would prevent the disease from spreading to other regions of the brain, which is associated with more severe dementia. This finding has important clinical implications. When tau is released into the extracellular space, it would be much easer to target the protein with therapeutic agents, such as antibodies, than if it had remained in the neuron."

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Columbia University Medical Center



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