The Role of Mitochondrial Dysfunction in Alzheimer's Disease | Dr. Elizabeth Yurth SSRP & AFA

The Seeds Scientific Research and Performance Institute hosted a day-long seminar featuring experts in nearly every facet of modern medicine with a focus on Alzheimer’s disease research. 

Importantly, the seminar was dedicated to raising funds to benefit the Alzheimer’s Foundation of America (AFA) and has collected $39,938 as of June 21, 2021.

Dr. Elizabeth Yurth, a founding faculty member of the SSRP, spoke on the Role of Mitochondrial Dysfunction in Alzheimer’s Disease. Before diving into her vast knowledge on the subject, Dr. Yurth shared a brief, touching story of her own experiences with Alzheimer’s disease in her family.

Her story speaks to the unfortunate truth that many in the field are so invested in Alzheimer’s research because of the impact it has had on their personal lives. The SSRP and AFA collaboration allowed a vast array of experts to share their knowledge, while raising money to benefit the AFA. 

Mitochondrial Dysfunction in Alzheimer’s Disease

As Dr. Yurth reminds us, the mitochondria is “really cool.” Even its inception, as a bacterial ancestor of the mitochondria which made its way into our ancestral cells, makes it a remarkable part of our physical existence.

Without the mitochondria, our cells would not be capable of producing energy. As our mitochondria naturally break down and perform less efficiently over time, we begin to see their ability to produce energy suffer.

The relatively new knowledge that the mitochondria has control over cell communication indicates that the mitochondria is even cooler – it controls the lifecycle and growth of cells with its mito-to-nucleus messaging.

Thus, nearly all disease seems to come down to some form of mitochondrial dysfunction. Cellular stress leads to the mitochondria to signal to the cell ways to alter itself to “fix” the problem. Once mitochondria lack the ability to create energy, their vital messages go unsent.

The relationship between mitochondrial dysfunction and Alzheimer’s disease arises as aging, cellular mutation, and neurotoxins begin to alter the mitochondria and its ability to function properly. This first step – the damage to the mitochondria – leads to problems like protein damage.

Aging itself leads to protein damage, like misfolded proteins, and the mitochondria typically responds to this issue by getting rid of bad proteins. Problems arise when the mitochondria becomes overwhelmed and itself is damaged, becoming unable to rid the harmful proteins.

The end result of advanced mitochondrial damage is a lack of appropriate energy (ATP) creation. One of the largest energy consumers in the body is the brain. With a lack of sufficient energy to feed the many processes taking place in the brain, the brain and cognition begin to decline. 

There are a significant number of negative processes occuring in the Alzheimer’s brain, including neuroinflammation, Tau hyperphosphorylation, and protein damage. However, mitochondrial damage may be the starting point for all these issues.

A potential solution? Getting rid of the dysfunctional mitochondria, which struggle to fix or eliminate damaged proteins. Studies in mice have shown that enhancing mitophagy (ridding dysfunctional mitochondria) allows the brain to function appropriately.

The ultimate takeaway is this: Mitochondria is a piece of the puzzle, but battling a disease like Alzheimer’s will take a combination of every technique we have to resolve the varying negative processes of this complex disease.

Ultimately, reintroducing collaboration to medicine is key. Putting aside the competitive nature of modern medicine will result in a collection of ideas that offer hope in battling Alzheimer’s disease.

We are all in the trench together. Collaborations like the SSRP and AFA will ultimately lead to outcomes that may indeed prove Alzheimer’s a far less formidable foe. 

Watch Dr. Yurth’s presentation, and if you’d like to donate to the AFA, click HERE.

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Published June 22, 2021
Categories: Brain Health
Tags: brain

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