Scientists Discover Potential Cure for Baldness: Here’s How It Works

When discussing hair removal options, many products promise quick fixes or a return to the hair’s original luster. Unfortunately, these claims often fall short, leading to subpar and temporary results.

Despite the fact that 80% of men experience male pattern baldness, our understanding of how to slow, halt, or even reverse this process has been limited until recently.

Fortunately, breakthroughs in science may reveal effective strategies to combat this issue.

The intriguing solution could involve freezing hair at extremely low temperatures to produce clones—yes, clones! Sci-fi enthusiasts, get ready to support this innovation.

What Causes Male Pattern Baldness?

The common misconception is that bald individuals lack hair entirely, but that’s not true. When hair is lost, it doesn’t disappear; instead, it shrinks.

“Baldness is a result of hair shrinking,” explains Paul Kemp, CEO of HairClone, a pioneering company dedicated to next-generation hair loss treatments. “The hair isn’t gone; it’s just becoming smaller and less visible.”

The shrinkage occurs due to a type of skin cell known as dermal papilla, which surrounds the base of hair follicles and is essential for hair formation, growth, and texture.

During hair loss, the number of these vital cells—typically around 1,000 per follicle—diminishes dramatically.

This loss is exacerbated by dihydrotestosterone (DHT), a potent derivative of testosterone that affects hair follicles differently across the scalp. Generally, dermal papilla cells on the top of the head are more susceptible to this process compared to those on the sides.

Recent research findings, published in Experimental Dermatology, explore how these skin cells differentiate during early embryonic development, suggesting a genetic basis for why some areas are more prone to hair loss.

“The dermal cells that are lost and those that remain originate from distinctly different populations,” Professor Kemp clarifies. “Essentially, where you experience hair loss can be likened to a ticking clock set from the moment your body begins to develop.”

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Why Cloning Hair Could Cure Baldness

With the loss of dermal papilla cells linked to baldness, researchers are racing to discover ways to replenish them. Hair cloning, also known as hair propagation, is gaining traction, thanks to frontrunners like HairClone.

This pioneering technology is not yet available in the UK or US, but if successful, it could come with a hefty price tag. Kemp notes, “While initial costs will be high, scaling up production should help lower prices, making it comparable to advanced hair transplant techniques.”

Unlike traditional hair transplants, hair cloning can be initiated before significant hair loss occurs, ensuring discreet treatment results.

Here’s how the process works:

1. Hair Root Collection and Preservation:

Healthy hair follicles are extracted from areas where hair is still growing and cryogenically preserved for later use. For optimal results, it’s crucial to gather these follicles while they are still young.

2. Cell Multiplication:

This step involves isolating and multiplying dermal papilla cells in a laboratory setting. As Dr. Jennifer Dillon states: “From one follicle, we can multiply these cells over 1,000 times, resulting in over a million cells.”

3. Replantation:

The cultivated dermal papilla cells are injected back into bald areas of the scalp, returning hair to its natural thickness and fullness. This step is awaiting regulatory approval, but initial clinical data is promising.

While banking hair follicles is currently possible globally, it comes with a significant cost.

What Other Treatments Are Available?

Although hair cloning is a buzz-worthy topic, it isn’t the sole treatment option. A study published in the Cosmetic Dermatology Journal suggests that fat cells harvested from the abdomen could regenerate hair. This method, known as autologous fat grafting (AFG), eliminates the need for cryogenic preservation.

AFG falls under stem cell therapy, using versatile cells that can transform into various cell types to meet regenerative needs. Instead of freezing hair cells, stem cells can be extracted from the patient’s body and directed to grow into hair cells, injected into the scalp just like in hair cloning.

Another innovative treatment in development is microRNA therapy, which fine-tunes gene expression to stimulate hair growth and has the potential to be applied topically, thus reducing invasiveness.

When Will These Treatments Be Available?

As with hair cloning, various stem cell and microRNA treatments are currently seeking clinical approval, potentially becoming available in the coming years. Despite the rising optimism for effective baldness treatments, Dr. Claire Higgins, a tissue regeneration expert at Imperial College London, warns that success in lab trials does not always translate to clinical effectiveness.

Dr. Higgins believes that understanding the specific reasons why some dermal papilla cells are more vulnerable to hair loss will be key in designing more effective treatments. “While we understand the physiological changes leading to hair loss, the underlying causes remain unclear.”

Optimistically, Kemp concludes that future generations will have revolutionary solutions for hair restoration, much like advancements in dentistry. “Rather than waiting for hair loss to occur, we envision a world where individuals can maintain their hair throughout life.”


About Our Experts

Dr. Paul Kemp is the Co-founder and CEO of HairClone. Previously, he led the development of the first multicellular therapy approved by the FDA, currently benefitting millions globally. He also serves as co-director for doctoral training in regenerative medicine at the University of Manchester.

Dr. Claire Higgins is a leading lecturer in Tissue Engineering and Regenerative Medicine at Imperial College London, focusing on hair follicles and skin regeneration.

Dr. Jennifer Dillon heads research at HairClone, specializing in the development of cell therapies for hair loss and possessing over a decade of experience in stem cell and cancer research.


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Source: www.sciencefocus.com

Discover an Excerpt from “Art Cure” by Daisy Fancourt: New Scientist Book Club Picks

Spending Time Painting in Cornwall, UK

Ashley Cooper/Alamy

Russell hesitated at the door, unsure whether to enter or not. This wasn’t his usual environment; he only came at the doctor’s suggestion.

His journey began with a stroke that disrupted blood flow to his brain, leading to significant challenges. He faced months of recovery, relearning skills he once took for granted. As time passed, he encountered severe back pain, lost his job, and struggled to maintain relationships, becoming depressed and overwhelmed by his situation.

When his doctor suggested eight weeks of art classes, Russell doubted the effectiveness of art as therapy. Still, feeling like he had nothing to lose, he stepped inside.

To his surprise, the first class was less intimidating than expected; he didn’t draw but observed fellow students. The calming ambiance and vibrant colors somewhat eased his anxiety. On his way home, he noticed a shift—his breathing was slower and more peaceful. The next week, he recognized familiar faces and started doodling in the garden shed during sleepless nights. By the third class, he had picked up a paintbrush. In the following weeks, he proposed a collaborative project: to paint portraits of his classmates.

I first met Russell early in the morning at a Manchester hotel. We were both preparing to appear on BBC Breakfast, where he would discuss the pioneering initiative of “prescription-based art” within the National Health Service. His experiences left me in awe of the transformation he underwent.

During his subsequent checkup, doctors were impressed with his progress; both his mood and pain levels had significantly improved. Art classes provided him with a sense of structure, something he had started to look forward to. His doctor reduced his medication, noting the improvement in his overall health and sleep quality.

As he neared the completion of his portrait series, he approached Gloucester Art Museum to host an exhibition titled “We’re All Mad Here.” The event drew fellow students and healthcare professionals, leading to requests for more commissioned works, including paintings of a nurse’s children.

Over the past decade, Russell Haynes has showcased his art throughout the UK—from Gloucester Cathedral to the Tower of London. His pieces are now highly sought after, often selling for thousands. He not only continues to create art but also teaches classes, receiving referrals from doctors. Remarkably, Russell has not taken any medication nor visited a doctor in over a year.

When I asked him about the impact of those initial art classes, he stated simply:

“They saved my life.”

This excerpt is from a work by Daisy Fancourt. Art Cure: The Science of How Art Changes Our Health (Cornerstone Press), part of the New Scientist Book Club’s March selection. Join us for a shared reading experience here.

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Source: www.newscientist.com

How Expanding Gene Editing Technologies Could Cure More Diseases

CRISPR-Cas9 Gene Editing Complex Diagram

Science Photo Library/Alamy

Imagine if postal workers could hand over flyers to volunteers on each block, who would then distribute them to neighbors. This approach could enable biologists to enhance gene editing for various medical conditions, significantly amplifying treatment effects.

The goal is to have each targeted cell replicate the gene editing machinery, subsequently passing it on to adjacent cells. This cascading effect can lead to transformative changes in the DNA of multiple cells, offering a breakthrough in treating genetic disorders.

In studies involving mice, Wayne Go and his team, including CRISPR pioneer Jennifer Doudna, successfully tripled the number of edited liver cells using this innovative method.

“We’re instructing the first cell to produce tiny lipid particles that carry the CRISPR machinery,” Ngo explained. “This transforms the cell into a factory, distributing these vital packets to surrounding cells.”

The first FDA-approved CRISPR treatment for sickle cell disease requires harvesting blood stem cells for editing outside the patient’s body, which makes it prohibitively expensive. However, many ongoing trials aim to develop methods for directly editing cells within the body, making treatments more accessible.

A major hurdle is delivering the CRISPR machinery to a significant portion of specific cells in the body. “To effectively cure sickle cell disease, about 20% of blood stem cells need to be edited,” Ngo noted. “Achieving that threshold has been challenging.”

Even if the initial delivery reaches only 10% of blood stem cells, local amplification could tip the scales to success by increasing that percentage to 30%.

To enable amplification, Ngo targeted proteins that assist in viral budding from cells. These proteins bind to cell membranes, forming small sacs or vesicles that can be transferred to other cells.

By linking the viral proteins to the CRISPR Cas9 editing protein, the Cas9 protein—which guides the gene editing process—can be encapsulated in vesicles and transported to neighboring cells.

In experimental tests, Ngo’s team injected a DNA sequence encoding the Cas9 viral protein into the livers of mice. Although only 4% of cells took up the DNA, they achieved a 12% overall gene edit rate.

Real-world applications of gene editing will utilize alternative delivery methods beyond pressure injection, which served only as proof of concept. “It’s not the most efficient method, but it demonstrates the potential of our system,” Ngo stated. “Tripling the amplification is a promising start, and we are actively exploring ways to refine our delivery systems to treat various diseases.”

This amplified gene editing approach not only enhances efficiency but could also allow for lower dosages, increasing treatment safety.

Researchers have been investigating vesicle budding strategies for many years. Gaetan Bourgeot of the Australian National University noted that Ngo’s team might be the first to validate these strategies in animal models for gene editing. However, Burgio emphasized the need for rigorous controls and validation of their results.

Current self-amplifying mRNA vaccines illustrate similar principles, where the delivered mRNA codes for mechanisms to produce more copies. This tactic aims to make vaccines safer and more cost-effective by reducing the required doses; however, the excess mRNA remains within the cells where it was produced.

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Source: www.newscientist.com

Can Gene Editing Cure Prion Diseases? | Insights from Cyworthy

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DNA molecules are essential carriers of genetic information, including partner molecules. RNA encodes the building blocks of life, specifically amino acids. Together, DNA, RNA, and amino acids form larger structures known as genes, which make up the genetic code for proteins that perform vital functions or contribute to other significant biomolecules.

Occasionally, the RNA within a gene may contain defects that can severely impact protein functionality. Such misfolded proteins, which can lead to fatal diseases, are known as prions. Researchers are optimistic that advancements in RNA editing technology, such as CRISPR, could provide treatment for prion diseases.

The possibility of this treatment has been known since scientists first identified bacteria using natural gene editing methods to combat viruses. Recently, medical researchers from institutions such as Harvard University, the Massachusetts Institute of Technology, and Case Western University conducted a pilot study to explore CRISPR’s effectiveness against prion diseases. The research team aimed to identify defective RNA regions within the genome and modify the corresponding genes. This process involved pinpointing the start and stop codons crucial for gene expression.

In laboratory experiments, scientists collected RNA from mice infected with human prion diseases. Utilizing CRISPR technology, they modified the defective RNA at the molecular level by inserting new start and stop codons to prevent replication. They employed sgRNA designed to produce non-functional proteins. Three versions of the sgRNA were tested: sgRNA, F-sgRNA, and F+E-sgRNA.

The researchers administered a medically approved vector, specifically an adeno-associated virus loaded with modified sgRNA, into mice infected with prion disease. They hypothesized that successful intervention would halt prion replication and prevent related disorders.

To evaluate this, scientists used two groups of mice, one experimental group receiving the modified sgRNAs and a control group receiving none. At ages 6 to 9 weeks, both groups were injected with various strains of human prion disease. Subsequently, only the experimental group was treated with sgRNA between 7 to 10 weeks old.

The mice were monitored for 92 to 95 weeks, recording behavioral changes, weight fluctuation, and lifespan. Post-experiment, researchers compared the health outcomes of both groups to determine the efficacy of the treatment. The findings were promising: treated mice exhibited nearly a 60% increase in lifespan compared to their control counterparts.

To assess the experiment’s success, researchers euthanized the mice post-study and analyzed their brains. They were particularly concerned with ensuring that the edited RNA targeted the proper genes, avoiding off-target editing that could lead to unpredictable outcomes. A thorough examination for possible side effects and abnormalities not linked to prion activity was conducted.

Additionally, they assessed the prion activity to confirm the impact of CRISPR on the targeted RNA strand, focusing on prion protein levels in mice. They observed that treated mice had prion protein levels 4% to 40% lower than those in the control group, with the F+E-sgRNA treatment yielding a 43% reduction in prion levels.

The research team concluded that CRISPR gene editing holds potential for combating prion diseases in mice. However, the significant off-target editing observed could present risks in human applications due to possible adverse effects. The researchers recommend future investigations continue using rodent models until more precise editing techniques are developed. Nevertheless, these results symbolize a meaningful advance toward potential treatments for prion ailments in humans.

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Man Surprises Doctors with HIV Cure Following Stem Cell Transplant

Human Cells Infected with HIV

Steve Gschmeisner/Science Photo Library

A man has become the seventh individual to rid himself of HIV after receiving a stem cell transplant for blood cancer. Notably, he was the second case among seven to receive stem cells that weren’t resistant to the virus, reinforcing the idea that resistant cells may not be essential for HIV treatment.

“Understanding that treatment can occur without this resistance offers us additional avenues for combating HIV,” remarks Christian Gabler at the Free University of Berlin.

So far, five individuals have been cleared of HIV following transplants from donors possessing mutations in both copies of a gene responsible for CCR5, a protein that HIV targets to infect immune cells. Scientists have drawn conclusions that having two copies of a mutation that eradicates CCR5 from immune cells is crucial for eliminating HIV. “It was previously thought that the use of HIV-resistant stem cells was key,” states Gabler.

However, last year, a sixth instance emerged, known as the Geneva patient, who was declared free of the virus. His infection persisted for over two years after receiving stem cells that lacked the CCR5 mutation, indicating that CCR5 might not be the complete narrative, though many scientists suggest that two years without viral infection may not suffice to confirm an actual cure, Gabler notes.

The recent cases bolster the hypothesis that the Geneva patient has indeed been cured. The research includes a male who received stem cells in October 2015 to address leukemia, a blood cancer characterized by uncontrolled growth of immune cells. At the time, the patient was 51 years old and was infected with HIV. During the treatment, he underwent chemotherapy to eliminate a majority of his immune cells, allowing the donor’s stem cells to generate a healthier immune system.

Ideally, the man would have received HIV-resistant stem cells; however, these were unavailable, leading doctors to use cells with one typical and one mutated copy of the CCR5 gene. During this time, the patient was undergoing conventional HIV care known as antiretroviral therapy (ART), a regimen of medications that suppress the virus to undetectable levels, preventing transmission and reducing the likelihood of donor cells becoming infected.

Approximately three years post-transplant, he opted to discontinue ART. “He felt that he had waited long enough after the stem cell transplant and believed his cancer was in remission, so he anticipated a positive outcome from the transplant,” Gabler explained.

Shortly thereafter, tests revealed no traces of the virus in the man’s blood samples. Since then, he has remained free of the virus for seven years and three months, qualifying him as “cured.” He holds the record for the second-longest duration HIV-free amongst the seven declared cases, achieving this status longer than some by around a dozen years. “It’s astonishing that a decade ago he was very likely facing death from cancer, and now he has conquered a terminal diagnosis of a lingering viral infection without any medication. He is in good health,” Gabler remarked.

This discovery challenges our perceptions of what it entails to treat HIV through this method. “We once believed that transplantation required a donor without CCR5, but now it seems that’s not the case,” points out Ravindra Gupta from the University of Cambridge, who was not part of the study.

It’s generally assumed that the success of such treatments hinges on the inability of the virus to hide within remaining immune cells of the recipient after chemotherapy, thus preventing infection or replication in the donor’s cells. “Essentially, you deplete the pool of host cells that the virus can infect,” argues Gabler.

Nevertheless, Gabler speculates that the latest cases imply a potential cure can be achieved as long as non-resistant donor cells can eliminate the recipient’s remaining original immune cells before the virus has a chance to spread. Such immune responses often arise from variations in the proteins that the two cell sets display. These, he notes, enable donor cells to recognize the remaining recipient cells as a threat that must be eradicated.

The findings indicate a wider array of stem cell transplants might offer the possibility of curing HIV than previously believed, including those that do not exhibit two copies of the CCR5 mutation, according to Gabler.

However, for this to be effective, several factors must align, such as the genetic compatibility between the recipient and donor to ensure the donor’s cells can swiftly eradicate the recipient’s cells. Additionally, in the most recent case, the man possessed one copy of the CCR5 mutation, which may have modified his immune cell dynamics throughout his body, aiding in the eradication of the virus, Gabler noted.

This suggests that most individuals undergoing stem cell transplants for HIV or blood cancers should ideally receive HIV-resistant stem cells, as emphasized by Gabler.

It’s crucial to recognize that individuals with HIV who do not have cancer will not gain from stem cell transplants, as these procedures are highly risky and prone to life-threatening infections, Gabler warns. Most experts agree that adhering to ART (typically taken in pill form daily) is substantially safer and more practical for halting HIV’s spread. This approach allows many to lead longer, healthier lives. Moreover, a newly available medication, lenacapavir, offers nearly complete protection against HIV with just two injections annually.

Despite this, research continues on treating HIV through gene editing of immune cells and exploring preventive vaccines.

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Source: www.newscientist.com

Revolutionary Method for Ending Pregnancy Nausea Quickly: Discover the Morning Sickness Cure

We have all experienced vomiting at some stage in our lives. Whether it’s due to a nasty bout of food poisoning or the well-known norovirus that infects the population episodically. And we can all agree that it’s scary.

But imagine what it would do to you physically, mentally, and emotionally if you were to expect constant nausea and vomiting at a critical stage in your life.this is the reality for them
4 in 5 women experience nausea and vomiting during pregnancy. Even mild cases can cause unpleasant symptoms such as nausea, loss of appetite, and vomiting.

for 3% of women develop a condition called hyperemesis gravidarum.things get worse and require hospitalization and treatment.

According to the Office for National Statistics, in 2022 this will result in: 20,000 women hospitalized.



But until recently, little was known about the causes of nausea and vomiting during pregnancy. Anecdotal evidence suggests that the more nausea and vomiting you have, the healthier your pregnancy, and even suggests that it is related to the number of babies you have.

However, real-world evidence shows this is not true. In fact, nausea and vomiting can vary widely in severity and pattern during pregnancy.

Often referred to as “morning sickness,” nausea and vomiting during pregnancy can occur at any time of the day or night. Usually it’s worse for the first 12 weeks, then it calms down. However, for many women, it lasts throughout the pregnancy.

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However, after more than 20 years of research in this field, a breakthrough has been made that identifies a causal relationship. This was promoted by Dr. Malena Fezo, a geneticist at the Keck School of Medicine at the University of Southern California.

Fezo was inspired to pursue this career after suffering from severe nausea and vomiting during her second pregnancy in 1999. She was unable to eat or drink without vomiting, and she rapidly lost weight and became so weak that she could no longer stand or walk.

However, doctors were skeptical that she might be exaggerating her symptoms to get attention. Fezo was eventually hospitalized and she miscarried at 15 weeks.

Fezo will conduct genetic research on previously pregnant women in collaboration with 23andMe, a private company that allows individuals to send samples of their DNA to determine health status and insights into their ancestry. did.

She identified a link with a woman who suffered from severe nausea and vomiting during pregnancy (requiring an intravenous fluid). and a variant of the gene encoding a protein named GDF15, a hormone that acts on the brain stem.

This association pinpointed the need for further research to understand the role of GDF15 protein in pregnancy.

GDF15 is secreted by the placenta during the first two trimesters of pregnancy. It also likely plays a role in preventing the mother from biologically rejecting the baby, which is essential to allowing the pregnancy to continue. However, GDF15 has been shown to regulate physiological body weight and appetite through the brain. This substance is produced in excess in cancer patients who suffer from severe appetite and weight loss.

In addition to previous research, research led by Fejzo and the University of Cambridge Professor Stephen O'Rahilly We found that the level of GDF15 was high. Seen in women with severe nausea and vomiting during pregnancy. However, the effects of this hormone appear to depend on the woman's susceptibility and her exposure to GDF15 before pregnancy. Women who received higher levels of exposure before pregnancy had higher levels of the GDF15 hormone but did not have symptoms of nausea or vomiting.

It has been hypothesized that long-term exposure to GDF15 before pregnancy may have a protective effect and reduce a woman’s sensitivity to the hormonal surge caused by fetal development.

This exposure relationship is very unique and provides more understanding and knowledge as well as the potential that women may be desensitized by increasing their exposure to hormones before pregnancy. It also suggests possible treatments. Just like some people treat food allergies with controlled exposure therapy.

Many of the common symptoms affecting women, such as nausea and vomiting during pregnancy, are poorly understood despite their very high incidence. Women’s healthcare is not a niche, and there is much to understand and learn through this type of research.

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Source: www.sciencefocus.com