Polar bears are rewiring their own genetics to survive a warming climate

         Reading the title of this article confused me at first but after going through it I am more invested in polar bears than I was when I was 10. With warming climates worldwide, polar bears are being forced to adapt, and this is showing in their DNA. This is believed to be the first documented case of environmental change driving genetic change (note for my answer on the final). 

 

        Researchers say that this is because warming sea temperatures reduce the amount of ice flows that polar bears can hunt off of, causing their need to diversify. 

        Even though polar bears are adapting to the world around them, they are still projected to go extinct within the next century. This is truly upsetting to me as polar bears are some of my favorite animals in the world. I will be doing my part and donating to  conservation funds and hoping that it is not too late. 

Dawson Fournier

Source: https://www.nbcnews.com/world/greenland/polar-bears-adapting-survive-warming-climate-rcna248805

Secondary: https://abcnews.go.com/International/polar-bears-rewriting-dna-survive-warming-arctic-study/story?id=128278604 

Misophonia Has Genetic Links to Anxiety And Depression, Study Reveals

             A recent study has shown that misophonia, a condition that makes sounds like chewing, grinding and snoring overly agitating and anxiety inducing, can be linked to inherited depression and anxiety. 

 

        Researchers in the Netherlands have found that genetic mood conditions like anxiety, depression, and PTSD susceptibility were all linked to having misophonia as well as chronic tinnitus. As someone who suffers from both misophonia and tinnitus this article was very concerning. However, I do not feel like I have any of the other conditions so that is good. 

        It makes sense though, that these things would be linked. The feeling that you get when you hear someone slurp a hot drink is similar to the feeling of dread you get in your stomach when you read the bill from your dentist. 

        Overall I found this article very fascinating and relatable but also it reminded me I need to be aware of the way I feel and how I react to the situations I am in.

 

Dawson Fournier

Source: https://www.sciencealert.com/misophonia-has-genetic-links-to-anxiety-and-depression-study-reveals

Secondary: https://my.clevelandclinic.org/health/diseases/24460-misophonia 

New Study Aims to Detect Illness in Babies Early

New Study Aims to Detect Illness in Babies Early 

 A new study is providing doctors with a promising way to identify rare but treatable illnesses in newborns long before any symptoms appear. They are using cutting-edge genomic sequencing on umbilical cord blood, in which researchers hope to identify up to 200 inherited conditions (Dias, 2025). Doctors working on the project say that catching these conditions early could change families’ lives who are preparing for a baby, allowing babies access to treatments months or even years earlier than would normally be possible (Dias, 2025).

   There are some concerns involving how they determine who has the illness. Because everyone carries genetic mutations that may never lead to illness, experts worry that screening newborns so early could lead to false positive results that would suggest a problem when there isn’t one. This could cause unnecessary stress, extra testing, and fear for new parents. Some have also raised concerns about how securely the babies’ genetic information will be stored and who will be trusted with access to it (Dias, 2025).

   Although this study has some downsides, it’s still an important step forward in caring for babies. If it works the way doctors hope, it could help stop serious health problems before they even begin.

Although the study has some downsides, I think it could really make a difference for babies’ health. If it works the way doctors hope, it might be able to prevent serious illnesses before they happen. At the same time, I can understand why some parents might feel nervous about their baby’s genetic information being used because it's such a recent study. 

If you want to learn more about the study and see the full research details, you can visit the study’s official website here: https://www.genomicsengland.co.uk/initiatives/newborns 

References:

Dias, A. (2025, November 26). Genomic study of Gloucestershire newborns “could be life-changing.” https://www.bbc.com/news/articles/c0l7lx119nzo

Genomics England. (2024). Newborn Genomes Programme. Genomics England. https://www.genomicsengland.co.uk/initiatives/newborns

Screwworm Returns, and What is Being Done to Fight it.

 This past summer, an article was published in the New York Times detailing the re arrival of screwworm in the United States. Screwworm, largely eradicated in the 1970s in the United States, has made a reappearance due to breaching a barrier in Panama, sparking concern from both the U.S. and Mexico. The parasite is a flesh eating maggot that feasts on the open wounds of animals. It affects mostly livestock, but can also spread to other animals including deer, rabbits, and even humans.

  

The issue is, this problem had already been solved before. In the 1950s, it was discovered that scientists could create sterile male screwworm flies and release them into areas that contained massive amounts of screwworm. This would severely decrease the population as the females would mate with the sterile males, thus decimating the population. A barrier was created and maintained from 2006 onward, until 2022 where said barrier was somehow broken through, causing screwworm to start to make its way back into Central and North America. This means that these companies that were making the sterile flies will need to heavily ramp up production to drive down the population of these invaders and send them away for good. To me, this article highlights that safety and attention to detail that is needed to work in the field of science. If something like this can happen once, there is nothing stopping it from happening again. We need to ensure that  careful attention is payed to everything, so that something like this, or worse, doesn't happen again.

Cannabis Dependence and the Science Behind it

 This paper takes a close look at why some people are more at risk for cannabis dependence than others, and a big part of the story comes down to genetics. According to the article, cannabis is one of the most commonly used drugs worldwide, but only a portion of users end up developing dependence. The paper points out that global use ranges from about 2.8% to 5.1%, and men consistently show higher rates than women. It also explains that dependence isn’t just about using cannabis often, it’s about having a strong internal drive to keep using it, even when it causes problems.

The researchers report that cannabis dependence is partly inherited, with genetics accounting for about 55% of the overall risk. In the paper, they highlight 14 specific genes that seem most tied to cannabis dependence, including ANKFN1, CHRNA2, and NCAM1. These genes are connected to brain signaling and neural functioning, which makes sense given that cannabis affects the brain’s reward systems. The authors also mention several “candidate genes,” like CNR1 and ABCB1, that might influence how the body responds to cannabinoids, though they note the evidence for some of these is still being sorted out.

Even with all of these genetic clues, the paper makes it clear that genes aren’t destiny. Environmental factors, personal experiences, stress, mental health, and even how early someone starts using cannabis all play a role. The authors suggest that future work should look not only at DNA itself but epigenetic changes, basically, how gene activity gets switched on or off, to better understand why dependence develops in some people and not others. It’s a reminder that cannabis dependence is complicated, and genetics are just one piece of the puzzle.

Original Article: https://psychpersonality.com.ua/en/journals/tom-24-2-2023/genetika-zalezhnosti-vid-kanabisu

Secondary Article: https://link.springer.com/article/10.1186/s12920-021-01035-5?utm_source=chatgpt.com

Labels: "Cannabis" "Addiction" "Inheritability" 

Findings point to path forward for treatment of rare genetic disease

Friedreich’s ataxia is one of those rare disorders that most people don’t hear about, but it’s incredibly serious for the families affected by it. It causes muscle weakness, nerve damage, and major problems with coordination — and the hardest part is that there’s currently no real treatment that stops the disease from getting worse. That’s why this new research from the Broad Institute immediately caught my attention.

The scientists discovered a potential way to work around the genetic defect instead of trying to fix it directly. In Friedreich’s ataxia, the body loses a protein called frataxin, which the mitochondria need to make energy. Without enough frataxin, the cells basically struggle to function. What the researchers did was run genetic screens to find other genes that could “compensate” for that loss. Surprisingly, they found a couple of proteins, especially FDX2 and NFS1, that, when adjusted, helped cells overcome the frataxin shortage.

What I really liked about this study is that it opens the door to treatments that don’t rely only on CRISPR or gene therapy. Instead, these new findings suggest that traditional drugs could target these alternative pathways and still have a big impact on symptoms. In animal models, boosting these proteins actually improved the disease features, which feels like a huge step forward considering how limited current treatment options are.

Genetics of Spina Bifida

 

This review is about spina bifida (SB) as a complex congenital disorder of the central nervous system, emphasizing its significant genetic component alongside environmental factors. The authors detail that while the complete cause is not fully understood, research has identified over 250 associated genes in mouse models, pointing to disrupted pathways like the planar cell polarity (PCP) pathway, signaling, and folate metabolism. In humans, SB is considered an omnigenic trait, involving a combination of variants in genes such as VANGL1, VANGL2, CELSR1, and TBXT, as well as genes involved in folate processing like MTHFR. The review also covers the critical role of maternal factors (diabetes, folate deficiency) and the well-established preventive effect of folic acid supplementation. Beyond genetics, the article discusses the pathophysiology of the "two-hit" injury model and the evolution of treatment from postnatal surgical closure to groundbreaking fetal surgery, culminating in the introduction of the first FDA-approved clinical trial using placenta-derived mesenchymal stem cells (PMSCs) to augment in utero repair.

In my opinion, this research paper powerfully illustrates the convergence of genetic discovery and clinical innovation in tackling a devastating birth defect. The genetic narrative is particularly compelling; it moves SB from a condition historically attributed to simple folate deficiency or birth injury to a complex neurogenetic disorder with an "omnigenic" architecture. Understanding that hundreds of genes can disrupt fundamental embryological processes like neural tube closure reframes our approach, shifting focus from a singular cause to a web of vulnerabilities. This genetic complexity explains why folic acid, while hugely preventive, is not a universal cure. The most exciting implication lies in the therapeutic frontier: this genetic understanding lays the groundwork for the pioneering stem cell trial discussed. By identifying the specific cellular and signaling pathways that fail, researchers can now rationally design regenerative strategies, like using PMSCs, to protect or repair the developing spinal cord. This marks a paradigm shift from merely closing a physical defect to attempting a biologically-informed restoration of function, offering real hope for improving outcomes beyond the current limits of fetal surgery alone.

References: 

1. Hassan, A.-E. S., Du, Y. L., Lee, S. Y., Wang, A., & Farmer, D. L. (2022). Spina Bifida: A Review of the Genetics, Pathophysiology and Emerging Cellular Therapies. Journal of Developmental Biology, 10(2), 22. https://doi.org/10.3390/jdb10020022 

2. Spina bifida: MedlinePlus Genetics. (n.d.). Medlineplus.gov. https://medlineplus.gov/genetics/condition/spina-bifida/ 

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Neuron zapping help us understand Parkinson's

    Scientists at Johns Hopkins Medicine have taken an important step toward watching neurons communicate in real time. Using a clever “zap-and-freeze” approach, the research team was able to stop brain tissue—first in mice, then in human, at the exact moment one neuron sends a message to the next. Their findings, published in Neuron, give a rare glimpse into the split-second events at the synapse, the junction where most forms of Parkinson’s disease are thought to originate. Because synaptic disruptions drive the majority of Parkinson’s cases, being able to capture this process as it unfolds could bring researchers closer to understanding how communication starts to break down.

                       

    To test the method, the team stimulated neurons with a tiny electrical pulse and immediately froze the tissue, preserving every structure for analysis. Remarkably, samples taken from patients undergoing epilepsy surgery showed the same rapid recycling of synaptic vesicles that appeared in mice—including the presence of Dynamin1xA, a protein that enables ultrafast membrane recovery. This parallel between species reinforces the value of mouse models for human brain research. The researchers now hope to use zap-and-freeze on tissue from individuals with Parkinson’s disease, with the goal of pinpointing exactly how these shift in affected neurons and ultimately guiding new ideas.