Researchers Find Healthy Mitochondria Can Combat Alzheimer’s
There are many debilitating diseases that afflict humans. We are faced with numerous afflictions that do not have a cure as of yet. One of the most commonly known is cancer, which includes a range of different types. We have effective means of treating and getting rid of cancer, but we have nothing to prevent it or cure it outright. Individuals with cancer have to go through numerous chemotherapies, which is costly and makes us weak.
As we age, we encounter more diseases because our bodies are getting weaker. We are more prone to common illnesses, like the cold or flu, and our immune system becomes less effective at combating bacterial or viral infections that never really bothered us before. Over time, our minds also become weaker. We become more forgetful and cannot focus as much as we did when we were younger.
It was only a few years ago that celebrities and people across the internet were raising awareness for amyotrophic lateral sclerosis (ALS) by doing the ice bucket challenge. ALS is one of many neurodegenerative diseases that can affect us when we get older. ALS is typically seen in individuals in their 50-60s but can appear earlier or later.
Neurodegenerative diseases are the result of a progressive loss of neurons via their death, loss of structure, or loss function. At the moment, these diseases are incurable. We do have treatments to slow them down, but nothing to get rid of them or prevent them.
Recently, researchers have looked into the relationship between the mitochondria and Alzheimer’s to see if a potential treatment or cure can be found because many Alzheimer’s patients tend to have dysfunctional mitochondria.
What Is A Mitochondria
The mitochondria are the power plant of the cell. It is an organelle within cells that generate energy molecules to power cellular functions. They are a kind of cell within a cell because they have their own double membrane and DNA that separates them from other organelles. It is thought that the mitochondria were a highly specialized bacteria that was engulfed by a eukaryotic ancestor and survived. It eventually formed a symbiotic relationship with the host and evolved to become a single species.
Mitochondrial DNA is very small compared to the DNA in our genome because, over time, most of the original mitochondrial DNA migrated to the main set of DNA to further connect the two. This means that detrimental things that happen to DNA in either our chromosomes or the mitochondria can lead to diseases and a weakened state.
Cells are capable of creating more mitochondria when they need more energy or inhibiting that growth when there is an energy surplus. Cells are also able to kill off old or dysfunctional mitochondria to prevent them from damaging the cell or other cells. Maintaining enough energy to carry out different cellular functions is important to the health of an individual and failure to do so can lead to many different kinds of diseases.
Mitochondrial diseases are the direct result of the mitochondria failing to perform its normal functions. There are many different types. There are also diseases that, while not caused by the mitochondria, are associated with mitochondrial defects because they result in an increased disease state and makes a disease worse. One such disease is Alzheimer, which is one of the reasons that researchers are looking at mitochondria to deal with it.
What Is Alzheimer’s
Alzheimer’s disease is a progressive neurodegenerative disease that results in memory loss and loss of other mental functions. It is the most common cause of dementia, which is a group of mental disorders resulting in the loss of social and cognitive skills important for daily function. Like other neurodegenerative diseases, Alzheimer’s is the continued loss of brain cells as they degenerate and die or lose functioning. This all leads to the symptoms that we see. Because this is a progressive disease, it becomes worse the longer it remains until it becomes fatal. Its symptoms may start off with minor confusing or difficulty remembering things, but as time goes on and more cells degenerate, the symptoms get worse.
While the disease is associated with aging, it is not an age-based condition and can affect individuals below 65 years of age in early-onset forms of the disease. Researchers believe that Alzheimer’s is caused by genetics, lifestyle, and the environment. Genetic factors increase your chance of getting the disease but rarely lead to it. Only 5% of Alzheimer’s cases are the direct result of genetic factors.
There are over 5 million people in the United States with Alzheimer’s and it is expected to reach over 16 million people by 2050. Since 2000, there has been an 89% increase in death related to the disease and it is expected to rise without any improved treatments or cures.
Alzheimer’s also creates a burden on the healthcare and social systems of the U.S. because individuals affected by the disease are in need of care from others. It is estimated that over $250 billion was spent on caring for individuals with the disease. With the anticipated increase in cases of Alzheimer’s, this number will probably increase.
There is currently no cure for the disease and treatment options are for slowing down and mitigating the symptoms for a certain amount of time. The other options are constant care for individuals. As Alzheimer’s continues to become a central part of health issues faced by people, research into a cure and better treatment continue.
A Potential Treatment
One of the treatment options for Alzheimer’s that is being heavily researched is the reduction in amyloid plaque formation. Amyloid plaques are characteristic of Alzheimer’s and are buildups of outside nerve cells in the brain. Because of the direct association with Alzheimer’s, researchers have been looking into but results are currently inconclusive.
Faced with this lack of results, researchers are looking into other avenues to find a cure. Researchers from the Ecole Polytechnique Fédérale de Lausanne, in Switzerland, decided to explore the disease as a metabolic condition rather than a neurodegenerative disease. They did so because the cells that degenerate in Alzheimer’s become unable to protect their mitochondria and remove any dysfunctional ones. This results in further cellular degeneration and increases the diseased state.
Since the mitochondria provide energy to the brain and everywhere else in the body, diseases that prevent their repair and turnover favor dysfunctional mitochondria. Understanding this, the researchers looked into how they can protect the mitochondria from becoming dysfunctional to see if it affected the disease.
The researchers examined the mitochondrial unfolded protein response (UPRmt), to protect the mitochondria under stress, and mitophagy, which is responsible for the mitochondrial death. They found that by activating these two factors of mitochondria of worms, the mitochondria were kept safe from dysfunction and dysfunctional ones died out. This leads to fewer amyloid plaques and created more healthy worms that performed better and lived longer than their non-activated counterparts.
The results are exciting because they showcase the important role of the mitochondria in Alzheimer’s as both a factor increasing the diseased state and a potential treatment or cure. While this needs to be tested in humans to see if the results will be similar, the researchers also tested the activation in mitochondria of cultured human cells and saw similar results.
As with any new research, more work is needed to support this finding before we can move on to humans to test. If successful, this treatment might be able to stop the progression or slow it down a lot. This would allow people to live longer and better as well as be the first step towards a cure.