A team of scholars of the Curtin University carried out a pioneering study by discovering one probable cause of Alzheimer’s disease. The discovery, of some scientific importance, will allow the development of both preventive therapies and more effective therapies against this terrible disease.
There Research was published in the prestigious scientific journal PLOS Biology.
Alzheimer’s disease: here’s what the study says
The research, which exploited mouse models, identified that a probable cause of Alzheimer’s was the leaking from the blood into the brain of particles carrying fat and toxic proteins.
Professor John Mamo, lead researcher of the Curtin Health Innovation Research Institute (CHIRI), said his research group of Australian scientists identified the probable “blood-brain pathWhich can lead to Alzheimer’s, the most widespread form of dementia globally.
“While we previously knew that the defining feature of people living with Alzheimer’s was the progressive buildup of toxic protein deposits within the brain called beta-amyloid, the researchers did not know where the amyloid came from, or why it was deposited in the brain“, Explained Professor Mamo.
“Our research shows that these toxic protein deposits that form in the brains of people living with Alzheimer’s most likely enter the brain by fat-carrying particles in the blood, called lipoproteins“The scientist specified:”This ‘blood-brain path’ is significant because if we can manage blood levels of lipoprotein-amyloid and prevent them from leaking into the brain, this opens up potential new treatments to prevent Alzheimer’s and slow memory loss.
Building on previous award-winning research which showed that beta amyloid is produced outside the brain with lipoproteins, Professor Mamo’s team tested the innovative “blood-brain path”By genetic engineering of mouse models to produce human liver of only amyloid which makes lipoproteins.
“As we had anticipated, the study found that mouse models producing lipoprotein-amyloid in the liver suffered from inflammation in the brain, accelerated brain cell death and memory loss“, Explained Professor Mamo.
“Although more studies are now needed, this finding shows that an abundance of these toxic protein deposits in the blood could potentially be addressed through a person’s diet and certain medications that could specifically target lipoprotein amyloid, thereby reducing their risk or slowing the progression of Alzheimer’s disease“.
Professor Warren Harding, president of Alzheimer’s WA, said the findings could have a significant global impact for the millions of people living with Alzheimer’s: “Having universities like Curtin working with the pharmaceutical industry is important if we are to tackle this devastating disease“Said Harding.
“In Australia, around 250 people are diagnosed with dementia every day, adding to the staggering half a million Australians already living with dementia. Without significant medical advances such as the breakthrough that Professor Mamo’s team has made, the number of Australians living with dementia is estimated to exceed one million by 2058. This has a significant impact on families, caregivers and communities. “
Previous research by Professor Mamo and his research group in this area was awarded the NHMRC-Marshall and Warren Award for the most innovative and potentially transformative research.
Currently, the team is conducting a clinical study, the Probucol in Alzheimer’s-clinical trial , which builds on previous findings that a historic cardiovascular agent reduces lipoprotein-amyloid production and supports cognitive performance in mice. The full article is titled “Liver proteins can cause Alzheimer’s disease in the brain ”.
Alzheimer’s disease: correlation with liver proteins
According to Mamo and his scientists the amyloid protein produced in the liver can cause neurodegeneration in the brain.
Since the protein is thought to be a key contributor to the development of Alzheimer’s disease (AD), the findings suggest that the liver can play an important role in the onset or progression of the disease.