Defective Mitochondria And Alzheimer’s Disease

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Alzheimer’s Disease (AD), a progressive neurodegenerative disorder that affects millions of people worldwide, is currently incurable.

Only the symptoms are treatable, and the medical community has poured billions of dollars into clinical trials trying to develop new treatments to slow down the disease.

Yet, while other fields of research such as cancer and HIV therapies make leaps in efficacy, new Alzheimer’s drugs continue to flop.

In the last decade, AD drug developers focused on eliminating a protein called amyloid-beta.

With an AD brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function.

However, recent research is finding amyloid-beta plaque buildup is more so a symptom of AD than a cause, and the focus going forward should be on the prevention of such.

A New Theory of How to Treat Alzheimer’s Disease.

In a new study in the scientific journal, Nature Neuroscience, an international team of researchers from the University of Copenhagen have come closer to unlocking a new way of attacking AD.

The new target focuses around a cleaning process in brain cells called mitophagy.

“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. 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,” says Vilhelm Bohr, author of the study and affiliate professor at the Center for Healthy Aging and National Institutes of Health.

How Mitophagy Keeps Alzheimer's Disease At Bay

Mitophagy is your body’s way of recycling defective mitochondria.

Mitochondria are the biological “powerplants” for every cell in the body and mitophagy makes sure new ones can replace those that have been damaged. 

Again, with both Alzheimer’s and other states of dementia, there is an accumulation of the protein amyloid-beta in the brain, which ultimately causes cells to die.

In these new animal models, the researchers show that when boosting mitophagy, such accumulation is slowed down.

In other words, by keeping the brains energy production high the proteins associated with AD are effectively recycled.

“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,” says Vilhelm Bohr.

This new research adds to the ever growing evidence that mitochondrial health is a key factor in living a disease free life.

More so, that keeping the mitochondria intact and efficient is often at the root of the problem instead of the obvious symptoms most medical treatments are distracted by.

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