Genetics Provide Clue to Culprits of Alzheimer's Disease
Researchers know that dementia is set to become an even greater public health concern than it is now. Indeed, Alzheimer's disease and other forms of dementia are set to cost society more than other expensive killers, like heart disease. However, despite the fact that Alzheimer's disease and dementia are undeniably problems, researchers have no idea how to treat the illness or even what causes it. Recent studies may have illuminated an answer for researchers.
According to the website Healthland, researchers have found two significant changes in the brain that are characteristic of Alzheimer's disease. The protein amyloid beta builds up in the brain, causing a sticky plaque that prevents nerve cells from performing their jobs; meanwhile, the tau protein also builds up in spinal fluid and the brain, causing issues with memory and cognitive ability.
A recent study published in the journal Neuron found that certain genetic markers can indicate the presence of a group of receptors in brain cells. Those receptors could either protect or boost the formation of the tau cells. By looking at the genomes of over 1,000 people, the researchers were able to discover that certain genes increased risk for Alzheimer's disease, increasing the speed at which nerves and tissue were damaged.
According to ABC Science, two recent studies shed some doubt on whether amyloid beta is a culprit for the neurological disorder at all. A study published in the journal PLoS One found that the plaques of amyloid beta that are characteristic of the illness do not appear until well after the symptoms of the disease begin.
"The conclusion of our study, taken together with other studies is that behavioural decline, neuronal cell death and inflammatory cell activation precede plaque deposition, providing a strong indication that neurodegenerative processes are occurring independent of amyloid-beta protein," the researchers write in the study.
Another study went even farther. The researchers found that amyloid beta was not a harmful effect on the brain, but had protective benefits. In a study conducted with mice models of multiple sclerosis, the protein was even able to reverse the paralysis characteristic of the condition.
"We were so fixated on the idea that amyloid is bad for the brain that if one goes back and looks at the old literature and the new literature, one finds there's a lot of publications where people have ignored these kinds of experiments in humans where, for instance, lower levels of amyloid are associated with earlier dementia," Stanford University professor Lawrence Steinman said to ABC Science.
That study was published in the journal Science Translational Medicine.