The Brain Cleanup Crew
As older Americans become a larger part of our population, we’ll see more people with Alzheimer’s dementia. In the next 30 years, the cases will double unless we find a cure. Studies tell us AD is linked to the dysfunction of a brain protein called tau that gathers inside neurons. Another protein called beta-amyloid damages neurons by covering them, like plaque on your teeth.
Scientists are now studying whether the cause of AD is that these proteins are piling up in the brain and cerebral spinal fluid because too few are being removed. Normally, specialized waste removal cells called tanycytes clear the brain of toxins. They’re unique because they lie between the bloodstream and the cerebral spinal fluid.
One of the proteins they move out is tau. Tau normally helps support a neuron’s internal structure, but in AD they become sticky and clumpy, killing the cell. To study the movement of tau, some were tagged with dye and injected into mice. Mice with impaired tanycytes accumulated tau in the brain while fewer tau was seen in the bloodstream.
This suggests tanycytes are vital in removing tau from the brain, and if they don’t work properly, too much of the tau protein accumulates in the brain. Too much tau triggers the body to make too much beta-amyloid, the other protein implicated in dementia. Studies show that people with AD do move less tau from the cerebral spinal fluid to the blood. Could therapies that target tanycytes hold the key to curing Alzheimer’s? We sure hope so.
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These brain cells clear proteins that contribute to Alzheimer’s
When specialized cells called tanycytes stop working, disease-causing tau proteins build up in the brain.
Little-Known Cells May Be Key to Clearing Alzheimer’s Proteins
For years, the buildup of tau protein has been identified as a primary driver of Alzheimer’s disease. Now, a study has uncovered the brain’s “waste management” secret: specialized cells called tanycytes. These rare, non-neuronal cells act as a shuttle, capturing toxic tau from the cerebrospinal fluid (CSF) and dumping it into the bloodstream for disposal. The research reveals that in Alzheimer’s patients, these tanycytes become fragmented and lose their ability to clear the “trash,” leading to the rapid accumulation of tau. This discovery shifts the focus from neurons to these structural shuttle cells as a potential new frontier for slowing neurodegeneration.
Tanycytic degeneration impairs tau clearance and contributes to Alzheimer’s disease pathology
In our aging societies, Alzheimer’s disease (AD) and other age-related cognitive disorders such as frontotemporal dementia (FTD) have become a major public health concern. Alzheimer’s disease (AD) is characterized by pathological tau protein accumulation in the brain and cerebrospinal fluid (CSF) instead of timely efflux into the blood. However, the underlying mechanisms are unclear. We show, using animal and cellular models and patient tissues, that tanycytes of the hypothalamic median eminence, which bridge the blood and CSF, are involved in tau transport and AD pathogenesis.