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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Como todo el organismo, el cerebro va madurando y envejeciendo a su propio ritmo, cambiando sus capacidades conforme avanzamos en edad. Primero consolidando y luego perdiendo facultades. Conociendo esto, podremos discernir entre lo normal y lo patológico. elpais.com/salud-y-bien...

elpais.com

Las cinco ‘edades’ del cerebro humano: hay cambios cruciales alrededor de los 9, los 32, los 66 y los 83 años

Un estudio identifica cuatro puntos de inflexión fundamentales en el desarrollo de las conexiones neuronales a lo largo de la vida, un hallazgo que puede ayudar a comprender alteraciones en la cognici...

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Link to full article: Wang, Ying Hekimi, Sigfried. Elevated cellular accumulation of endogenous and exogenous CoQ by altered intracellular trafficking. Journal of Biological Chemistry, Volume 0, Issue 0, 110878 www.sciencedirect.com/science/arti...

sciencedirect.com

Elevated cellular accumulation of endogenous and exogenous CoQ by altered intracellular trafficking

Coenzyme Q (CoQ) is produced in the inner membrane of mitochondria, from where it is transported to other cellular membranes. Cellular CoQ levels drop…

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

The study concludes that cells regulate CoQ levels not only by synthesis but through trafficking, recycling, and lysosomal processing. Targeting these pathways could one day help patients with CoQ deficiencies by boosting cellular CoQ without relying solely on supplements.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Then came a key discovery: inhibiting lysosomal function—either blocking acid lipase (Lalistat-1) or preventing lysosomal acidification (Baf-A1)—also increased cellular CoQ. That means the lysosome is involved in CoQ degradation or recycling. When blocked, more CoQ accumulates.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Because synthesis didn’t seem to explain the findings, the authors tested whether COQ biosynthesis proteins changed. Most COQ proteins were unchanged. COQ7 even decreased with iron, meaning synthesis was not being ramped up. Trafficking remained the main suspect.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Interestingly, iron did not globally increase ROS levels, even though its effect was redox-sensitive. This means the mechanism isn’t driven by oxidative stress but by subtle intracellular redox interactions that affect CoQ handling rather than damage pathways.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

The team explored whether this effect depends on redox biology. Using NAC, an antioxidant, they found that NAC significantly reduced the CoQ-boosting effect of iron and paraquat. Both iron and a ROS-generating compound elevated CoQ, supporting a redox-linked mechanism.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

To test how cells handle external CoQ10, they supplied CoQ10 in micelles and then added iron. Iron massively increased the accumulation of this exogenous CoQ10 beyond either treatment alone. So iron improves both endogenous and imported CoQ retention.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

To see whether iron was boosting CoQ by increasing its production, the team measured CoQ inside mitochondria, where it’s made. Iron barely changed mitochondrial CoQ while whole-cell CoQ rose sharply, pointing to changes in trafficking rather than synthesis.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

The effect of iron happened fast, becoming clear within hours. Even more interesting, when iron was removed, CoQ levels dropped back to normal, showing the boost is reversible. This suggests dynamism, not permanent metabolic rewiring.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

The researchers worked with several cell types, including RAW264.7 macrophages, and supplemented them with ferrous iron (Fe²⁺). Surprisingly, iron rapidly and strongly increased total cellular CoQ—much more than expected if synthesis alone were responsible.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/11/2025

Coenzyme Q is essential for energy production and antioxidant defense, but cells can lose it when synthesis drops. This new study explores an unexpected idea: instead of increasing CoQ production, what if we could boost CoQ by changing how cells traffic and recycle it?

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

Applications are now open. Please spread the word to motivated students and early-career researchers. More details will be available soon on the ICQA webpage. This is a unique opportunity to join a high-level program shaping future experts in skin ageing. icq10a.com

icq10a.com

International Coenzyme Q10 Association

The International Coenzyme Q10 Association is a nonprofit association, which aims to promote research on the biomedical aspects of Q10.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

Labs, supervisors and institutions are encouraged to share this opportunity. It’s a rare chance for young scientists to explore both academic and industrial research, gaining skills that bridge fundamental biology with real-world innovation.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

The course is especially relevant for the CoQ10 research community, offering insights into mitochondrial pathways and the functional role of CoQ10 in skin biology. It provides valuable knowledge for anyone working on oxidative stress and ageing.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

Selected students receive a €2,000 scholarship, and Beiersdorf fully covers accommodation and meals in Hamburg. This makes the program accessible and reduces financial pressure, allowing participants to focus on training and scientific growth.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

The program welcomes Master students, PhD candidates, and postdocs interested in ageing, mitochondria, redox biology or skin science. Previous experience is helpful but not essential—curiosity, motivation, and commitment are what matter most.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

This initiative is educational, not commercial, and aims to promote collaboration between universities and industry. Only twelve highly motivated participants will be selected, ensuring close mentorship and a truly immersive scientific experience.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

What makes this program special is its dual setting: one month in Ancona for academic training, followed by three months in Beiersdorf’s Hamburg labs. Participants work on a real industrial project, experiencing both scientific and applied research.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

The course explores the mechanisms of skin ageing with a strong focus on redox biology, mitochondrial health, and CoQ10 pathways. Students will gain advanced insights into how oxidative stress shapes cellular function and how CoQ10 supports skin physiology.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

The first edition was highly successful, bringing students into a unique environment where academic research meets industrial innovation. This new edition continues that mission, offering deep scientific training blended with real-world applications. www.beiersdorf.com/career/stude...

beiersdorf.com

Unique Program with Polytechnic University of Marche in Ancona

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 24/11/2025

Great news for students and young researchers! The Polytechnic University of Marche, together with Beiersdorf, is launching the 2nd edition of an advanced course on skin ageing, oxidative stress, mitochondrial dysfunction, and the biology of CoQ10.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

These results are promising but preliminary, since they come from fibroblasts, not patients. Still, the study highlights mitochondria as a key player in Rett syndrome and supports exploring early, mutation-specific CoQ10 strategies in future research.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

Overall, Rett fibroblasts show oxidative stress, mitochondrial imbalance and CoQ10 deficiency. Ubiquinol helps some mutation types but not all, indicating that genetic background shapes how cells respond and whether supplementation is meaningful.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

The study examined PON2, an antioxidant enzyme that interacts with CoQ10. In the most stressed cells, PON2 levels were slightly higher but its activity was reduced, suggesting dysfunction. This enzyme may become a useful biomarker for Rett syndrome.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

Mitochondrial structure was also altered. One mutation displayed abnormal increases in both fission and fusion proteins, suggesting chaotic remodeling. Ubiquinol shifted dynamics toward balance in some cells, but not in the severely affected line.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

They then measured reactive oxygen species in mitochondria and the cytosol. Some mutations produced far more ROS than controls. After ubiquinol, two cell lines improved, but one with a C-terminal deletion showed no benefit, remaining highly stressed.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

But quantity is not everything. Researchers checked the oxidized fraction of CoQ10, a marker of oxidative stress. Rett cells had a heavily oxidized pool, but ubiquinol lowered this burden, showing a partial restoration of redox balance after treatment.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

The team treated all fibroblasts with ubiquinol, the reduced and active form of CoQ10. Every patient cell line absorbed it, with the most deficient cells showing the largest recovery. This suggests a mutation-linked vulnerability in CoQ10 handling.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

When measuring CoQ10 at baseline, one mutation showed a striking deficiency, while others also had reduced levels. Since CoQ10 is vital for energy and antioxidant defense, this shortage may worsen cellular stress and contribute to Rett dysfunction.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

Researchers collected skin fibroblasts from girls with different MECP2 mutations and compared them to healthy cells. Fibroblasts are ideal because they contain mitochondria, allowing a direct view of cellular energy, redox balance, and oxidative stress.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/11/2025

Rett syndrome is a rare disorder mainly affecting girls, and scientists are trying to understand why cells struggle to produce energy. A new study looks at mitochondria in patient-derived fibroblasts and uncovers a clear imbalance tied to CoQ10 levels.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Want to dive deeper into the data? Check out the full open-access study by Meza-Torres et al. (2025) in Antioxidants: www.mdpi.com/2076-3921/14.... A must-read for anyone interested in CoQ biology, aging, and mitochondrial resilience. #OpenScience #CoenzymeQ

mdpi.com

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Takeaway: Aging erodes our CoQ factories; exercise can shore them up, resveratrol helps a bit, but effect depends on tissue. Future therapies could target Coq gene regulation directly. Thoughts on translation to humans?

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

This work lays a foundation for therapeutic strategies focused on enhancing endogenous CoQ production—via transcriptional and lifestyle modulation—rather than relying solely on supplements.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

The authors suggest combining lifestyle (exercise) with nutraceuticals (resveratrol or other modulators) could best preserve CoQ biosynthesis with age, delaying mitochondrial dysfunction and oxidative damage.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Exercise appears as a more robust stimulus for CoQ gene network maintenance—especially in high-energy tissues like muscle and heart. Resveratrol adds benefit but is less potent.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Why is this important? CoQ is central to OXPHOS and antioxidant defense. Its decline may contribute to age-related loss of mitochondrial resilience, higher oxidative stress, and decline in organ function.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

The study emphasizes that supporting CoQ-synthome expression is crucial—not all benefits come from supplementing CoQ externally. Building intrinsic machinery matters.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Interestingly, brain and kidney were less responsive to both interventions. This hints at tissue-specific regulation of CoQ biosynthesis and perhaps limited reversibility in certain organs.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Exercise training upregulated several Coq genes in muscle and heart—more consistently than resveratrol—and boosted CoQ levels where gene expression increased, especially in cardiac tissue.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Resveratrol (in drinking water) partially restored Coq transcripts in muscle and liver—but effects were tissue-specific and modest. Transcriptional rescue didn’t always translate to higher CoQ levels.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

Result: most Coq genes decline steadily with age—especially in muscle and brain—mirroring drops in CoQ content. This suggests aging impairs CoQ-synthome integrity, reducing CoQ supply and cellular antioxidant capacity.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

They measured transcripts of Coq genes (Coq2–Coq9) in skeletal muscle, heart, liver, kidney, and brain—from young to old mice—while also measuring CoQ9 and CoQ10 levels in each tissue.

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 25/07/2025

What happens to coenzyme Q (CoQ) production machinery in aging tissues—and can resveratrol or exercise reset it? Meza Torres et al. tracked expression of the “CoQ synthome” and CoQ levels in mice across ages and interventions.⬇️

mdpi.com

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/07/2025

RTN4IP1 is no longer a black box. With collaborative science, we’re piecing together the puzzle of mitochondrial disease—one gene at a time. What other secrets do our mitochondria hold? 🔬✨ #Genetics #Mitochondria #CRISPR #Science #RTN4IP1 #CoenzymeQ #LeighSyndrome

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/07/2025

It also shows why time matters in biology. Signals lost in noise become patterns when viewed over time. In mitochondrial science, that’s a game changer. 🔑📊

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/07/2025

This work has real-world impact: it can improve diagnostics for rare disorders, uncover hidden disease mechanisms, and eventually support tailored therapies. 🏥🧬

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/07/2025

Their time-resolved approach didn’t just catch essential genes—it captured regulators and assembly factors with subtle effects that traditional screens would miss. A dynamic roadmap of mitochondrial function! 🗺️

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INTERNATIONAL COENZYME Q10 ASSOCIATION @icq10a.bsky.social · 17/07/2025

Another gene, ECHS1, was also flagged. Though known for fatty acid metabolism, it turns out ECHS1 regulates mitochondrial function independently, affecting key enzymes like pyruvate dehydrogenase. 🧠🧪

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