THE HUMAN BRAIN is an incredible, complex web of connections. Cells called neurons send signals from region to region, and their communication allows us to do everything from forming thoughts to accessing memories.
But for nearly 6 million Americans, neurodegenerative diseases like dementia, chronic traumatic encephalopathy (CTE), and Alzheimer’s disease prevent neurons from functioning properly. The progressive memory loss that characterizes these diseases is well-known. Yet the mechanisms that cause them—and ways to treat them—are still poorly understood. That’s partly because neurodegenerative diseases have different causes. CTE can be triggered by repeated head trauma, while fronto-temporal dementia is caused by a genetic mutation, and Alzheimer’s can be triggered by environmental, genetic, and behavioral factors. But all of these diseases are characterized by malfunctions in two proteins found in neurons: beta-amyloid and tau.
Now, scientists are starting to understand more about how tau could trigger and spread disease. In a paper published last week in Cell, researchers at the Buck Institute for Research on Aging detailed the “interactome” of tau, showing all the proteins it comes into contact with. That information offers new insights about how dysfunctional tau affects the cell and how it can travel from neuron to neuron, possibly seeding disease throughout the brain.
Tau is a protein that helps stabilize the internal skeleton of n
Tau is a protein that helps stabilize the internal skeleton of nerve cells (neurons) in the brain. This internal skeleton has a tube-like shape through which nutrients and other essential substances travel to reach different parts of the neuron.
THE HUMAN BRAIN is an incredible, complex web of connections. Cells called neurons send signals from region to region, and their communication allows us to do everything from forming thoughts to accessing memories.
But for nearly 6 million Americans, neurodegenerative diseases like dementia, chronic traumatic encephalopathy (CTE), and Alzheimer’s disease prevent neurons from functioning properly. The progressive memory loss that characterizes these diseases is well-known. Yet the mechanisms that cause them—and ways to treat them—are still poorly understood. That’s partly because neurodegenerative diseases have different causes. CTE can be triggered by repeated head trauma, while fronto-temporal dementia is caused by a genetic mutation, and Alzheimer’s can be triggered by environmental, genetic, and behavioral factors. But all of these diseases are characterized by malfunctions in two proteins found in neurons: beta-amyloid and tau.
Now, scientists are starting to understand more about how tau could trigger and spread disease. In a paper published last week in Cell, researchers at the Buck Institute for Research on Aging detailed the “interactome” of tau, showing all the proteins it comes into contact with. That information offers new insights about how dysfunctional tau affects the cell and how it can travel from neuron to neuron, possibly seeding disease throughout the brain.
(wired.com)
Tau is a protein that helps stabilize the internal skeleton of nerve cells (neurons) in the brain. This internal skeleton has a tube-like shape through which nutrients and other essential substances travel to reach different parts of the neuron.
The tau proteins (or τ proteins, after the Greek letter with that name) are a group of six highly soluble protein isoforms produced by alternative splicing from the gene MAPT (microtubule-associated protein tau). They have roles primarily in maintaining the stability of microtubules in axons and are abundant in the neurons of the central nervous system (CNS). They are less common elsewhere but are also expressed at very low levels in CNS astrocytes and oligodendrocytes.