New Treatments Emerging for Migraine Sufferers

 A canceled dinner, another missed workday, an afternoon spent waiting for the room to stop feeling too bright and too loud. For people living with migraine, the impact reaches far beyond head pain. And when familiar medications offer little relief, it’s easy to assume that managing the condition means simply enduring it. Fortunately, migraine treatment has changed considerably in recent years. Medicines developed specifically for migraine, along with devices and other approaches, are giving patients more options to discuss with their doctors. 

Dr. Crystal Jicha, a UCI Health neurologist who specializes in migraine and other headache disorders, emphasizes that getting the right diagnosis is an essential starting point. Migraine is a neurological condition, and recognizing its symptoms can help people receive appropriate care.

A tension headache commonly feels like pressure or a tight band around the head. Migraine attacks can bring pain severe enough to interrupt ordinary activities, often accompanied by nausea, vomiting, or sensitivity to light and sound. Some people also find smells difficult to tolerate. 

Others experience an aura: temporary neurological symptoms that may include shimmering lines, blind spots, or tingling sensations. Not everyone with migraine experiences aura, and symptoms can vary between people and even between attacks. There is no single blood test or brain scan that confirms migraine. Doctors generally make the diagnosis through a medical history, symptom assessment, and examination, ordering tests when needed to investigate other causes. 

One of the biggest changes in treatment has come from understanding a substance called calcitonin gene-related peptide, or CGRP. This naturally occurring chemical messenger plays a role in the pain pathways involved in migraine. Newer medications target either CGRP itself or the receptor it acts on, helping interrupt those signals.

For years, many preventive treatments came from medicines originally developed for other conditions, including certain blood-pressure medicines, antidepressants, and antiseizure drugs. Those treatments can still be useful. CGRP therapies have expanded the choices by offering medications designed specifically around migraine biology. 

There are two different treatment goals to understand: 

Acute treatment is used to relieve an attack when it occurs. 

Preventive treatment is taken on a schedule to reduce how often attacks happen and, in some cases, how severe they are. 

 Depending on the medication, CGRP treatments come as tablets, injections, intravenous infusions, or a nasal spray. Some treat attacks, some prevent them, and certain medicines can serve either purpose under an appropriate prescribing plan. The formulation and schedule depend on the particular drug. 

The American Headache Society considers CGRP therapies a first-line option for migraine prevention. That means patients do not necessarily need to try and fail older preventive medicines before these treatments can be considered medically appropriate. However, a professional recommendation does not guarantee insurance coverage. Individual plans may still impose requirements or restrictions.

These medicines are not the answer for everyone. Benefits, side effects, other health conditions, medication interactions, cost, and personal preferences all matter when choosing treatment. Someone who dislikes daily tablets may prefer a less frequent treatment, while another person may strongly prefer an oral medicine. 

Medication is also only one part of migraine care. Devices that use electrical or magnetic stimulation to influence nerve pathways offer another option. Known as neuromodulation devices, they may help treat attacks, prevent them, or both, depending on the device. Some require a prescription, and availability, suitability, and insurance coverage vary. 

Regular sleep, adequate hydration, consistent meals, and stress-management techniques can also support treatment. Cognitive behavioral therapy and mindfulness may help some people manage symptoms and the burden of living with recurring attacks. These approaches do not imply that migraine is imagined or simply caused by stress; they are additional ways to manage a complex neurological condition. 

A headache diary can make appointments more useful. There’s no need for an elaborate system: a notebook, calendar, or phone app can work. Record when symptoms occur, how long they last, how disruptive they are, which treatments you use, and whether those treatments help. Note possible contributing factors, such as disrupted sleep or missed meals, without assuming that every attack must have an identifiable trigger.

You do not have to wait until migraine takes over your life to ask for help. 

Recurring attacks that interfere with work, family responsibilities, or social activities deserve medical attention. So do symptoms that persist despite treatment. A primary care clinician can assess the problem and, when appropriate, refer you to a neurologist or headache specialist. 

Researchers are also investigating treatments beyond CGRP. One promising target is another signaling molecule called PACAP. Experimental medicines that block this pathway have shown encouraging results in clinical trials, but they remain under investigation. More research is needed to establish their benefits, risks, and eventual place in migraine care. 

There is still no cure for migraine, and finding an effective treatment can take patience. But an unsuccessful treatment years ago does not mean today’s options will offer the same result. If your current approach leaves you regularly missing out on everyday life, a fresh conversation with your doctor may reveal possibilities you haven’t yet tried.

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Breakthrough new treatment can help millions recover their lost hair

Scientists have uncovered a tiny molecule with the potential to transform hair loss treatments. Researchers at North Carolina State University have identified a microRNA, miR-218-5p, that plays a key role in hair follicle regeneration. By regulating a critical growth pathway, this molecule could open the door to more effective therapies.

For millions struggling with hair loss, available treatments often fall short. Surgical procedures can be invasive, while chemical solutions frequently fail to deliver lasting results.

Despite common belief, hair follicles don’t vanish in balding areas—they shrink. Scientists now believe that restoring dermal papilla (DP) cells in these areas could help hair follicles regain function.

A research team led by Ke Cheng at NC State set out to tackle this problem. They grew DP cells in two ways: a traditional 2D culture and a more advanced 3D spheroid model. Unlike flat cultures, the 3D spheroids better mimic the cells’ natural environment, potentially improving their regenerative abilities.

To test their approach, the team conducted an experiment using mice. They compared three treatments: 2D-cultured DP cells, 3D spheroid DP cells embedded in a keratin scaffold, and Minoxidil, a widely used commercial hair growth product.

The differences were striking. In just 20 days, mice treated with 3D spheroid DP cells had regrown 90% of their hair, reaching that milestone by day 15.

“The 3D cells in a keratin scaffold performed best,” Cheng said. “The spheroid mimics the hair microenvironment, and the keratin scaffold acts as an anchor, keeping the cells where they’re needed.”

Further analysis revealed why the 3D spheroid DP cells were so effective. They released exosomes rich in miR-218-5p, a microRNA that amplifies a crucial growth pathway for hair follicles. When levels of this molecule increased, hair follicles became more active. When it was blocked, hair growth slowed or stopped entirely.

“Cell therapy with the 3D cells could be an effective treatment for baldness, but you have to grow, expand, preserve and inject those cells into the area,” Cheng said. “MiRNAs, on the other hand, can be utilized in small molecule-based drugs. So potentially you could create a cream or lotion that has a similar effect with many fewer problems. Future studies will focus on using just this miRNA to promote hair growth.”

The Emotional Impact of Hair Loss

Hair loss affects millions of people, causing both physical and psychological distress. It can result from genetics, hormonal changes, medications, or medical conditions, leading to insecurity and low self-esteem.

While treatments like minoxidil and finasteride can slow or halt hair loss, they do not always result in regrowth. Hair transplant surgery, though an option, is expensive and carries risks such as scarring and infection.

The potential impact of this research is significant. Hair loss can profoundly affect an individual's self-esteem and quality of life. Developing new and effective treatments can improve the lives of millions.

Identifying miR-218-5p as a candidate for drug development marks an important step forward. The next steps involve conducting further studies to determine the safety and efficacy of miR-218-5p-based treatments for hair loss. The hope is to create treatments that are less invasive and more effective than current options, offering new hope to those affected by hair loss.

The research by North Carolina State University on miR-218-5p opens new avenues for treating hair loss. By focusing on the molecular pathways involved in hair follicle regeneration, this study provides a promising outlook for developing non-invasive treatments that could significantly improve the quality of life for millions suffering from hair loss.

The research appears in Science Advances, and was supported by the National Institutes of Health and the American Heart Association. Cheng is corresponding author. Postdoctoral researcher Shiqi Hu is first author.

 

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Discovery about how cancer cells evade immune defences inspires new treatment approach

A recent discovery about the process of evasion by cancer cells has led researchers towards a new approach to treat the disease.

Cancer cells are known for spreading genetic chaos. As cancer cells divide, DNA segments and even whole chromosomes can be duplicated, mutated, or lost altogether. This is called chromosomal instability, and scientists at Memorial Sloan Kettering have learned that it is associated with cancer's aggressiveness.

The more unstable chromosomes are, the more likely that bits of DNA from these chromosomes will end up where they don't belong: outside of a cell's central nucleus and floating in the cytoplasm.

Cells interpret these rogue bits of DNA as evidence of viral invaders, which sets off their internal alarm bells and leads to inflammation. Immune cells travel to the site of the tumour and churn out defensive chemicals. A mystery has been why this immune reaction, triggered by the cancer cells, does not spell their downfall.

"The elephant in the room is that we didn't really understand how cancer cells were able to survive and thrive in this inflammatory environment," said Samuel Bakhoum, a physician-scientist at MSK and a member of the Human Oncology and Pathogenesis Program.

According to the new study from Dr. Bakhoum's lab in the journal Cancer Discovery, the reason has to do, in part, with a molecule sitting on the outside of the cancer cells that destroys the warning signals before they ever reach neighbouring immune cells.

The findings help to explain why some tumours do not respond to immunotherapy, and -- equally important -- suggest ways to sensitize them to immunotherapy.

Detecting Dangerous DNA

The warning system Dr. Bakhoum studies is called cGAS-STING. When DNA from a virus (or an unstable cancer chromosome) lands in a cell's cytoplasm, cGAS binds to it, forming a compound molecule called cGAMP, which serves as a warning signal. Inside the cell, this warning signal activates an immune response called STING, which addresses the immediate problem of a potential viral invader.

In addition, much of the cGAMP also travel outside the cell where it serves as a warning signal to neighbouring immune cells. It activates their STING pathway and unleashes an immune attack against the virally infected cell.

Previous work from the Bakhoum lab had shown that cGAS-STING signalling inside of cancer cells causes them to adopt features of immune cells -- in particular, the capacity to crawl and migrate -- which aids their ability to metastasize. This provided part of the answer to the question of how cancer cells survive inflammation and aid metastasis in the process.

The new research shows how the cancer cells cope with the warning signals that activated cGAS-STING releases into the environment. A scissor-like protein shreds the signals, providing a second way the cells can thwart the threat of immune destruction.

The scissor-like protein that coats cancer cells is called ENPP1. When cGAMP finds its way outside the cell, ENPP1 chops it up and prevents the signal from reaching immune cells. At the same time, this chopping releases an immune-suppressing molecule called adenosine, which also quells inflammation.

Through a battery of experiments conducted in mouse models of breast, lung, and colorectal cancers, Dr. Bakhoum and his colleagues showed that ENPP1 acts like a control switch for immune suppression and metastasis. Turning it on suppresses immune responses and increases metastasis; turning it off enables immune responses and reduces metastasis.

The scientists also looked at ENPP1 in samples of human cancers. ENPP1 expression correlated with both increased metastasis and resistance to immunotherapy.

Empowering Immunotherapy

From a treatment perspective, perhaps the most notable finding of the study is that flipping the ENPP1 switch off could increase the sensitivity of several different cancer types to immunotherapy drugs called checkpoint inhibitors. The researchers showed that this approach was effective in mouse models of cancer.

Several companies -- including one that Dr. Bakhoum and colleagues founded -- are now developing drugs to inhibit ENPP1 on cancer cells.

Dr. Bakhoum says it's fortunate that ENPP1 is located on the surface of cancer cells since this makes it an easier target for drugs designed to block it.

It's also relatively specific. Since most other tissues in a healthy individual are not inflamed, drugs targeting ENPP1 primarily affect cancer.

Finally, targeting ENPP1 undercuts cancer in two separate ways: "You're simultaneously increasing cGAMP levels outside the cancer cells, which activates STING in neighbouring immune cells, while you're also preventing the production of the immune-suppressive adenosine. So, you're hitting two birds with one stone," Dr. Bakhoum explains.

The pace of the research has been incredibly fast, he says. "One of the things I would be really proud of is if this research ends up helping patients soon, given that we only just started this work in 2018."

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