What’s New in Psychology?
A Cause Found for Alzheimer’s Disease?
Jim Windell
We know that Alzheimer's disease is a progressive neurologic disorder that causes the brain to shrink and brain cells to die. And we are aware that Alzheimer's is the most common cause of dementia. And that about 5.8 million people in the U. S. who are over 65 live with Alzheimer's disease.
Furthermore, most of us know that among the early signs of the disease include forgetting recent events or conversations. But as the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.
But what we don’t know is exactly what causes the dreaded neurological disease.
However, ground-breaking new research from Curtin University in Perth, Australia may have discovered a possible cause of Alzheimer's disease.
This new study, published in the PLOS Biology journal and tested on mouse models, has identified that a probable cause of Alzheimer's disease is the leakage from blood into the brain of fat-carrying particles transporting toxic proteins.
Building on previous award-winning research from a research team at Curtin that showed beta-amyloid is made outside the brain with lipoproteins, lead investigator from the Curtin Health Innovation Research Institute (CHIRI) Director Professor John Mamo and his team tested the “blood-to-brain pathway” by genetically engineering mouse models to produce human amyloid-only liver that make lipoproteins.
“As we predicted,” Professor Mamo says, “the study found that mouse models producing lipoprotein-amyloid in the liver suffered inflammation in the brain, accelerated brain cell death and memory loss.”
Mamo explains that although scientists 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, what they didn’t know was where the amyloid originated from – or why it deposited in the brain.
“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 blood, called lipoproteins,” adds Mamo.
Although further studies are needed to learn more about this blood-to-brain pathway, this research shows that 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. Diet and drugs could possibly reduce the risk of Alzheimer’s, or could slow its progression.
“This blood-to-brain pathway is significant because if we can manage the levels in 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,” concludes Professor Mamo, who along with his research team's previous research in this area was awarded the NHMRC-Marshall and Warren Award for the most innovative and potentially transformative research.
To read the original article, find it with this reference:
Virginie Lam, Ryusuke Takechi, Mark J. Hackett, Roslyn Francis, Michael Bynevelt, Liesl M. Celliers, Michael Nesbit, Somayra Mamsa, Frank Arfuso, Sukanya Das, Frank Koentgen, Maree Hagan, Lincoln Codd, Kirsty Richardson, Brenton O’Mara, Rainer K. Scharli, Laurence Morandeau, Jonathan Gauntlett, Christopher Leatherday, Jan Boucek, John C. L. Mamo. (2021). Synthesis of human amyloid restricted to liver results in an Alzheimer disease–like neurodegenerative phenotype. PLOS Biology, 19 (9): e3001358 DOI: 10.1371/journal.pbio.3001358