Human brain is an amazingly complex, interconnected network. Cells called neurons send signals from one region to another, and their communication allows us to do everything from forming thoughts to accessing memories.
But almost 6,000,000 won Americans, neurodegenerative diseases like dementia, chronic traumatic encephalopathy (CTE), and Alzheimer’s disease prevents nerve cells from working properly. The progressive memory impairment that characterizes these diseases is well known. However, the mechanism that causes them – and how to treat them – is still poorly understood. That’s partly because neurodegenerative diseases have different causes. CTEs can be activated by repetitive head trauma, while temporal dementia is caused by genetic mutations, and Alzheimer’s disease can be caused 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 beginning to understand more about how tau can cause and spread disease. In an article published last week in Cabinet, Researchers at the Buck Institute on Aging have detailed tau’s “interaction system,” showing all the proteins it comes into contact with. That information provides new insights into how dysfunctional tau affects cells and how it can travel from neuron to neuron, possibly seeding pathogens. throughout the brain.
“These types of studies provide us with insight into the disease process at the molecular level,” said Tara Tracy, an assistant professor at the Buck Institute and lead author of the paper. “That’s the goal of all these studies, to get more information for things that can be targeted to slow progress.”
Over the past few decades, scientists have focused on beta-amyloid, which forms clumps around the outside of cells and blocks communication between them. The theory is that if scientists can figure out how to destroy those tumors – or prevent them from appearing in the first place – the disease can be brought under control.
But after years of development, several drugs that target beta-amyloid have become available mostly fail to improve patient outcomes. Last year the US Food and Drug Administration granted fast approval to Aduhelm, The first such treatment was approved since 2003, but it extremely expensive and has been criticized by doctors saying it inefficient prevent disease progression. A lot of great health systemincluding Massachusetts General Hospital, Cleveland Clinic and Department of Veterans Affairswill not prescribe it.
Focusing on other proteins involved in neurodegenerative diseases could help scientists find new ways to treat them. “Proteins don’t work in isolation,” says Nicholas Seyfried, an associate professor of biochemistry and neurology at Emory University who studies neurodegeneration. He says that the more scientists understand how these malfunctioning proteins affect cells, the more treatment options there will be.
What causes tau to go from a normal protein to a diseased protein is sometimes a mystery. For patients with frontotemporal dementia, this is due to change gene. But for people with other illnesses, what causes tau to initiate misbehavior is still unknown. In the case of CTE, it can be the result of repetitive head trauma. In Alzheimer’s disease, environmental factors such as air pollution or blood vessel problems that prevent blood from flowing to the brain may play a role. Regardless of the trigger, diseased tau proteins eventually build up the clumps. Unlike beta-amyloid, these increase in of nerve cells.
