Targeting the cleaning system in brain cells known as mitophagy could offer a new way to attack Alzheimer’s disease, according to new research.
“When the cleaning system does not work properly, there will be an accumulation of defective mitochondria in the brain cells. And this may be really dangerous,” says study author Vilhelm Bohr, affiliate professor at the Center for Healthy Aging and National Institutes of Health.
“At any rate, the poor cleaning system is markedly present in cells from both humans and animals with Alzheimer’s. And when we improve the cleaning in live animals, their Alzheimer’s symptoms almost disappear.”
The researchers have looked more closely at the cleaning process in brain cells from deceased Alzheimer’s patients, in Alzheimer’s-induced stem cells, and in live mice and roundworms with Alzheimer’s. In addition, they’ve also tested active substances targeted at the cleaning process in the animal models.
“It significantly strengthens our results that the cleaning process seems to be important in both human cells and across different animal species. And then it is encouraging that in living animals we are able to improve the central Alzheimer’s symptoms, memory, and learning,” Bohr says.
The mitochondria lie inside the cell and work as the cell’s energy factories. Mitophagy breaks down defective mitochondria and reuses their proteins. Researchers know from previous studies that dysfunctional mitophagy is associated with poor function and survival of nerve cells, but so far, aren’t sure about the connection to Alzheimer’s.
In both Alzheimer’s and other dementia, there is an accumulation of the proteins tau and beta amyloid in the brain, leading to cell death. In the new animal models, the research shows that boosting the mitophagy slows the accumulation.
Researchers believe the findings indicate that the cleaning process may offer a way to treat Alzheimer’s, but they need to do further investigation and plan to start clinical trials in humans in the near future.
Additional researchers from the University of Copenhagen, the University of Oslo, and the National Institutes of Health contributed to the work, which appears in Nature Neuroscience.
The Helse Sør Øst RHF (the Southern and Eastern Norway Regional Health Authority), the Research Council of Norway, the ERC, and the Olav Thon Foundation funded the work. Nordea-Fonden supported the Center for Healthy Aging research.
The researchers have a research and development agreement with ChromaDex and Elysium Health.
Source: University of Copenhagen
