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Gender-Specific Beneficial Effects of Docosahexaenoic Acid Dietary Supplementation in G93A-SOD1 Amyotrophic Lateral Sclerosis Mice.

(Or…Managing the Unmanageable: Diet as Therapy)

In summer 2014–a year before I began graduate studies–the ice bucket challenge splashed across social media. Participants were filmed getting drenched with ice-cold water. Videos typically ended with nominations for others to join the ice bucket dunk or donate money towards ALS research. Within a month, the ALS Association received over 100 million USD.

ALS (Amyotrophic lateral sclerosis, Lou Gehrig’s disease) is characterized by progressive death of motor neurons within the brain and spinal cord. Broken motor neuron-muscle signalling results in loss of voluntary movement, eventually leading to death.

A (no) MYO (muscle) TROPHIC (nutrition)

ALS has no cure. Following diagnosis, half of ALS patients die within the next five years…although there are notable exceptions (theoretical physicist Dr. Stephen Hawking and NFL athlete Steve Gleason). In 1990, members of the World Federation of Neurology gathered in Spain to define the diagnostic criteria of ALS. Almost 30 years later, the Ayala lab at Institut de Recerca Biomèdica in Lleida, Spain explores how diet might improve ALS outcomes.

In November 2019 Dr. Ayala’s team published their work in Neurotherapeutics. I was able to participate in this project and, in October, I visited with members of Dr. Victoria Ayala’s lab (including lead author Dr. Pascual Torres). The Ayala Lab utilized a mouse model of ALS (G93A-SOD1) to examine the impact of dietary DHA (docosahexaenoic acid) supplementation. DHA is a fatty acid that contributes to neurocognitive development, anti-inflammatory responses, and lipid signalling. We consume DHA through our diet–key food sources include eggs, algae, fish, and nuts/seeds. ALS patients, however, display a decrease of DHA within the spinal cord.

Torres et al. report that DHA supplementation improves life expectancy and motor capabilities (stride length) in male, but not female, mice. DHA supplementation also increases DHA levels within the spinal cord of male mice. The authors suggest that increased DHA mitigates systemic inflammation likely improving ALS outcomes. A cautionary note: the G93A-SOD1 mice model genetic (familial) ALS–SOD1 gene mutations are linked to ALS. However, the majority of ALS cases have no known genetic component. Intriguingly, ALS is more common in males than females. This research highlights the importance of assessing disease pathology and putative treatments in males and females.

Questions to ponder:

Could DHA help manage specific cases of ALS? If so, what basic research/clinical trials would be needed to assess DHA efficacy? What are the limitations and/or benefits of mouse research? Are there additional mechanisms that might explain why DHA supplementation improves ALS outcomes in the G93A-SOD1 model?

Check out the publication to learn more about ALS research in the Ayala Lab. To donate to the ALS Association click here.

Thoughtful exploring,

-KCB

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Me in Lleida (La Seu Vella cloisters)–stay tuned for more discussion re: international collaborations!

By KCBauer

Hello! My name is KCBauer and I am a PhD candidate at the University of British Columbia. I am a researcher, writer, musician, and explorer. Originally from Washington DC, I graduated with a BA in Music and BS in Biology in 2014. This blog focuses on the gut microbiota, the trillions of microorganisms that reside along the digestive tract. My grad research at UBC examines the role of the gut microbiota on human health, brain development, and anthropology. When I am not in the lab, I enjoy ambling through Vancity, listening to music, reading science journals, and hiking. If you have questions, ideas for blog topics, suggestions for place to visit in BC, or corrections send me an email at KCBauer@msl.ubc.ca.

2 replies on “Gender-Specific Beneficial Effects of Docosahexaenoic Acid Dietary Supplementation in G93A-SOD1 Amyotrophic Lateral Sclerosis Mice.”

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