Scientists Discover How Brain Cells Die in Alzheimer’s in Breakthrough Study
A breakthrough in Alzheimer’s research has finally answered a question scientists have been asking for years. Scientists have discovered how brain cells die when people develop Alzheimer’s, a study published in Science revealed.
“This is a very important and interesting finding,” researcher Bart De Strooper, from the UK Dementia Research Institute, told the BBC. He continued, “For the first time, we get a clue to how and why neurons die in Alzheimer’s disease. There’s been a lot of speculation for 30-40 years, but nobody has been able to pinpoint the mechanisms.” Researchers from Belgium and the UK transplanted human brain cells into the brains of genetically modified mice, who were programmed to produce large quantities of abnormal amyloid.
The research found that the disease progresses through necroptosis — a kind of cellular suicide.
People who suffer from Alzheimer’s lose brain cells and experience a build-up of abnormal proteins called amyloid and tau, which leads to the symptoms of the disease, including memory loss.
Amyloid is “a protein that is found in our brains and bodies, but in Alzheimer’s disease, amyloid sticks together and forms different sized clumps that later become plaques in the brain,” according to Alzheimers.org.
Tau is a protein that “forms insoluble filaments that accumulate as neurofibrillary tangles in Alzheimer’s disease and related tauopathies,” the National Library of Medicine explains.
But it wasn’t until the recent breakthrough that scientists understood why this build-up occurs.
The research team responsible now believes that the abnormal amyloid begins to build up in the spaces between the neurons, causing brain inflammation which results in a change to the internal chemistry.
As the tangles of tau accumulate, the brain cells begin producing Maternally Expressed Gene 3 molecules, which triggers necroptosis.
Once the researchers understood this development, they were able to assist the brain cells’ survival by blocking the MEG3. De Strooper noted that this discovery could lead to a “whole new line of drugs development.” Experts note that these findings are a huge leap forward but will likely take years to be implemented into medicine.
The president of the British Neuroscience Association, Tara Spires-Jones of the University of Edinburgh, told the BBC that this research “addresses one of the fundamental gaps in Alzheimer’s research” and noted that “these are fascinating results and will be important for the field moving forward.”
But she clarified that “many steps are needed” until this work can help patients diagnosed with the progressive disease.
