A mouse study on the role of a protein in Alzheimer’s Disease produces some counterintuitive findings.
In 1906 Dr Alois Alzheimer did a post-mortem examination on the brain of Auguste Deter, a woman in her fifties whose death was preceded by a slow descent into dementia. Using the recently developed Bielschowsky staining technique, the Bavarian psychiatrist discovered something never seen before.
Lodged inside the nerve cells were clumps of tissue that looked a bit like black cotton, coiled into random shapes.
They are called neurofibrillary tangles, and are now known to be symptomatic of Alzheimer’s disease, which afflicts up to 70% of the nearly 350,000 people living with dementia in Australia.
Those little clumps are also known as “tau tangles”, after the protein that forms them.
Now our understanding of tau, and its role in the cause and potential treatment of Alzheimer’s disease, has been given a significant boost by new research published in the journal Nature Neuroscience.
The researchers, led by Benjamin Wolozin at the Boston University School of Medicine, US, had previously shown that when pathological tau accumulates in a brain cell culture, it goes hand in hand with another change.
There is also proliferation of so-called “stress granules”, tiny bundles of proteins that appear in cells stressed by things as diverse as viruses, toxins, temperature change and starvation.
One particular protein that makes up stress granules is called T-cell intracellular antigen 1 (TIA1). It can modify the cell’s response to stress and, ideally, enhance its viability.
Read the full article in Cosmos magazine here