The research, which was reported in the famous PLOS Science magazine and evaluated on mice model, found that fat-carrying nanoparticles moving hazardous protein through the bloodstream into the brains is a likely source of Alzheimer’s dementia.
A recent study conducted by Curtin has identified a possible source of Alzheimer’s dementia, an important discovery that could contribute to novel preventative and treatment options for the second-leading source of mortality.
A New Study Identifies An Alzheimer’s Cause
“While we previously knew that the hallmark feature of people living with Alzheimer’s disease was the progressive accumulation of toxic protein deposits within the brain called beta-amyloid, researchers did not know where the amyloid originated from or why it deposited in the brain,” Professor Mamo said.
It is notable here that the disease of Alzheimer’s is one of the ailments troubling millions of people across the globe, and this research may help the experts to have a novel way of treating the patients.
One of the team members mentioned that the research is still in the primary phase, but it has provided some excellent results, and hence further research will be much required to reach a better method for treatment of this ailment.
Professor John Mamo, Director of the Curtin Health Innovation Research Institute (CHIRI), claimed his joint team of scientists had discovered the likely ‘blood-to-brain pathway’ that may lead to Alzheimer’s illness, the most common type of dementia worldwide.
“Our research shows that these toxic protein deposits that form in the brains of people living with Alzheimer’s disease most likely leak into the brain from fat-carrying particles in the blood called lipoproteins.
“This ‘blood-to-brain pathway’ is significant because if we can manage the levels in the blood of lipoprotein-amyloid and prevent their leakage into the brain, this opens up potential new treatments to prevent Alzheimer’s disease and slow memory loss.”
Professor Mamo’s group examined the floor ‘blood-to-brain route’ by genetically modifying mice animals to develop humans amyloid-only liver that produces low-density lipoprotein, expanding on prior winner work that demonstrated beta-amyloid is formed beyond the brains with low-density lipoprotein.
“As we predicted, the study found that mouse models producing lipoprotein-amyloid in the liver suffered inflammation in the brain, accelerated brain cell death, and memory loss,” Professor Mamo said.
Adjunct Professor Warren Harding, Chairman of Alzheimer’s W.A., said the findings might have a big worldwide effect on the thousands of individuals who have Alzheimer’s illness.
“Having universities like Curtin working with the pharmaceutical industry is important if we are to tackle this devastating disease,” Mr. Harding said.
“While further studies are now needed, this finding shows the abundance of these toxic protein deposits in the blood could potentially be addressed through a person’s diet and some drugs that could specifically target lipoprotein amyloid, therefore reducing their risk or slowing the progression of Alzheimer’s disease.”
“In approximately 250 people are diagnosed with dementia daily, adding to the staggering half a million people who are already living with dementia. Without significant medical advances like the breakthrough Professor Mamo’s team has made, it is estimated that the number of people living with dementia will exceed one million by 2058. This has a significant impact on families, carers and communities.”
The NHMRC-Marshall and Warren Prize for most original and possibly transformational work was given to Professor Mamo and his study group for earlier work in this field.
The group is now undertaking a human experiment called Probucol in Alzheimer’s Disease, which would be predicated on prior discoveries that a historical cardiac drug reduces the lipoprotein-amyloid formation and improves mental function in mice.
The full paper is titled “Protein from the liver may cause Alzheimer’s disease in the brain.”
