Radically different
Nature Medicine, Published online: 10 July 2026; doi:10.1038/s41591-026-04497-1
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Ties van der Meer doesn’t know how many siblings he has.
The 47-year-old was conceived at a private fertility clinic in the Netherlands using sperm provided by an anonymous donor. After the Netherlands banned anonymous donation in 2004, the doctor who ran the clinic destroyed records that might have identified those donors, he says.
He describes the situation as “problematic.” Children have a right to know their biological parents, he says. While he did ultimately track down one sibling, who helped him identify his father along with other genetic relatives, he may have others he’ll never find.
Other donor-conceived people who have been able to track down siblings have found they have tens or even hundreds of them. One donor-conceived woman who found 25 half-siblings over the course of seven years told the Guardian, “It does make you feel a bit mass-produced.”
We need international limits on the number of children a single donor can contribute to, a European fertility organization argued yesterday. At a conference in London, members laid out plans to start with a Europe-wide limit.
Today many countries, including the UK, have banned anonymous egg and sperm donation. But anonymity can’t be guaranteed even in places where it is technically allowed. Genetic tests offered by companies like Ancestry and 23andMe, along with genetic registries, have made it much easier for donor-conceived people to find parents and siblings who share their genes.
And because sperm can be frozen and stored for years before it is eventually used, the current set-up can result in situations where donor-conceived people discover the identity of a genetic parent only after the person’s death. They might also find that they have siblings of very different ages, all around the world.
Some people are finding hundreds of siblings. Sperm from Jonathan Meijer, a Dutch man who began donating in 2007, was used to conceive between 550 and 600 children. (Stichting Donorkind, a foundation and advocacy group for donor-conceived people that’s chaired by van der Meer, took him to court, and he was ordered to stop donating in 2023.)
Stories like these can be distressing for donor-conceived people. And there are other reasons why limits are considered important. The offspring of a prolific donor might be at risk of unknowingly forming romantic or sexual relationships, for instance. And some people are concerned that a donor with a harmful genetic mutation might pass that down to many children.
This is unlikely, given the level of screening that most donors undergo. But it has happened. A man who donated his sperm to a sperm bank in Denmark was found to have a genetic mutation that significantly increased the risk of multiple cancers. But his sperm had already been used to conceive at least 197 children across Europe. Some of those children developed cancer. Some died.
Many countries already have legal limits for donors. In Malta and Cyprus, for example, both egg and sperm donors are allowed to contribute to the birth of just a single child, according to data presented at the European Society of Human Reproduction and Embryology (ESHRE) meeting in London on July 8.
Other countries set limits based on the number of families a single donor can contribute to, allowing recipients to have children who share a genetic link. In the UK, that limit is set at 10 families per donor.
But these limits are difficult to enforce, partly because donated gametes don’t necessarily stay in their original country. In Denmark, the national limit is set at 12 families. But the country is a major exporter of sperm. In the UK, for example, more than half of sperm donations in 2020 were imported—with most of those coming from either Denmark or the US.
“The only thing that really makes sense is a transnational limit,” Jackson Kirkman-Brown, a professor of reproductive biology at the University of Birmingham, said at the meeting.
Kirkman-Brown and his colleagues have spent months putting together a document that represents ESHRE’s position on these limits. After consulting with fertility specialists, clinics, sperm and egg banks, donors, and donor-conceived people, the team has developed a plan to start with a Europe-wide limit on sperm and egg donations.
ESHRE is calling on sperm and egg banks, as well as fertility clinics, to respect an initial limit of 50 families per donor. That’s still very high, according to a handful of people I spoke to at the meeting. But at least it’s a start.
Europe should move toward setting limits at 15 families per donor, Kirkman-Brown said. “We may find that 15 is also too high,” says Vasanti Jadva, who studies the psychological well-being of people conceived using donated eggs, sperm, and embryos at City St George’s in London. “We still don’t know what the right number is.”
It will be difficult to enforce these limits, too. And if they end up limiting the supply of donor sperm, there’s a chance that some people will turn to unregulated sperm donations from people who do not undergo health screening. Unregulated donations can lead to other problems for prospective parents, including the possibility that donors will seek parental rights over the children conceived using their sperm.
And it will be even harder to establish international limits. When I asked the American Society of Reproductive Medicine for its thoughts on ESHRE’s proposed limits, a representative directed me to a guidance document saying “it has been suggested” that for a population of 800,000, single donors should be limited to “no more than 25 births” in order to avoid the risk that relatives will have children together. (Considering the US has a population of over 340 million, the total figure could be pretty high, but many sperm banks opt to limit the number of families contributed to by a single donor at around 25.)
van der Meer thinks that even a limit of five families from a single donor would be high. International donation makes it even harder for donor-conceived people to connect with genetic relatives, so the limit for international contributions should be set at two families, he says.
Still, he thinks ESHRE’s suggested limit is a “positive first step.” Van der Meer has managed to track down a sibling, his father, and nephews, aunts, and uncles. He hopes that future policies respect the rights of donor-conceived children to know, and be in contact with, their genetic relatives.
“But,” he says, “you have to start somewhere.”
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In March, the Medicare Payment Advisory Commission (MedPAC) released its annual report to Congress on Medicare payment policy. The data related to physician payment are clear: By every metric we track, primary care in America is succeeding, and it has been for years. Nearly all Medicare beneficiaries have a primary care provider (PCP). Over three-quarters can see their PCP within two weeks. Patients in rural environments have less trouble finding a PCP and even shorter wait times. Services and spending on evaluation and management codes are increasing, and compensation among PCPs is rising faster than the rest of the field.
Yet this runs counter to the pervasive narrative that investing more in primary care is the key to solving the American health care crisis.
NEW YORK — A couple of years ago, a reporter approached the Boys’ Club of New York looking to interview some of its middle-schoolers for a story about the mental health crisis in boys.
It’s easy to see why. Many of the about 2,500 boys who participate in the 150-year-old organization’s after-school and weekend activities come from disadvantaged socioeconomic backgrounds, often living in single-parent households or facing the threat of immigration enforcement. With limited access to academic and developmental support, the risk factors are plentiful.
Jeremy Faust cuts through a hallway of Boston’s Brigham and Women’s Hospital on his way to see a patient who is struggling to breathe. It’s the start of his evening shift, and the emergency department hums with ambient sound: bleeping monitors, the rumbling wheels of medical carts, the squeaky soles of hustling staff. People on gurneys line the corridor, some wincing in pain, others chatting with relatives.
On this Wednesday evening in May, Faust is working what is typically a quieter shift, as far as emergency departments go. Still, he is overseeing a team of doctors, students, and physician assistants, and will tend to more than two dozen patients before signing off for the night.
It’s an understatement to say Faust likes to keep busy. Minutes earlier, he’d posted an article on his influential Substack newsletter, Inside Medicine, providing an update on a major international news story. An alert sent to the newsletter’s nearly 85,000 subscribers announced his “scoop”: Twenty-six passengers aboard the MV Hondius, the hantavirus-hit cruise ship docked at the time off Cape Verde, had disembarked much earlier than previously known — raising the possibility they could spread the rare virus in the United States.
Scientists have found that damaged myelin sheaths lead to abnormal rhythms in brainwave activity during sleep. These findings could have major implications for the development of biomarkers and therapies for neurodegenerative diseases that affect myelin, such as multiple sclerosis (MS) or Alzheimer’s disease.
“The myelin sheath helps electrical signals travel efficiently through brain circuits,” said Mohit Dubey, PhD, senior scientist at the Netherlands Institute for Neuroscience, who presented the study at the Federation of European Neuroscience Societies (FENS) Forum 2026. “We wanted to understand whether myelin damage could also affect how brain circuits behave during sleep. By studying this link, we hope to better understand what causes sleep disturbances in neurological disease and whether sleep-related brain signals could serve as biomarkers for diseases that are yet to show clinical symptoms, as well as showing disease progression.”
Although sleep is known to play a key role in brain health, its study has often been overlooked in the context of neurodegenerative diseases. In conditions like Alzheimer’s, sleep disruptions are known to contribute to fatigue and cognitive decline, especially during the REM sleep phase, which is critical to preserve healthy cognition and memory.
“Sleep disturbances are extremely common in neurological diseases such as multiple sclerosis and Alzheimer’s disease, but the biological reasons for these problems remain poorly understood,” said Dubey. “Understanding the biological link between sleep and brain circuit dysfunction could help guide future strategies for improving sleep and brain health in these conditions.”
Dubey’s team had previously shown that loss of myelin sheaths cause abnormal spikes of brainwave activity in the brain during sleep that seemed to resemble those observed in epilepsy and Alzheimer’s. In the current study, the researchers compared electroencephalogram (EEG) recordings of MS patients during sleep with mouse models of damaged myelin and Alzheimer’s. In both humans and mice, myelin loss resulted in similar abnormal bursts of brain activity during non-REM sleep phases and slower brainwave rhythms during REM sleep.
“REM is a stage of sleep associated with dreaming and replay of daytime experiences. In this state the brain produces rhythmic electrical patterns called oscillations that help coordinate communication between neurons,” said Dubey. “Our findings show that these rhythms become disrupted and slower when myelin degenerates, and that the electrical spikes seen during sleep are closely linked to the stability of brain circuits affected by neurodegenerative diseases such as MS and Alzheimer’s.”
While there are no treatments that can repair damaged myelin, some MS drugs are able to slow down the immune system’s attack on myelin sheath to reduce or halt disease progression. Further research to determine how exactly myelin damage alters brainwave patterns during sleep could aid the early detection of myelin degeneration and inform the design of therapeutic approaches that target myelination.
“This opens new research directions exploring how sleep rhythms depend upon the myelination status of the brain circuits,” said Dubey. “Sleep recordings may provide a non-invasive way to detect early changes in brain circuit myelination in neurological disease. This could eventually help clinicians monitor disease progression, and we want to investigate whether sleep recordings could be used as biomarkers to detect early changes in brain circuit function.”
The post Sleep Brainwaves Could Reveal Early Signs of Alzheimer’s and Multiple Sclerosis appeared first on Inside Precision Medicine.
As one of the most aggressive blood cancers, the way acute myeloid leukemia (AML) is classified continues to shape every major clinical decision—from risk stratification to the choice of targeted therapies. For decades, that classification has rested almost entirely on the gene mutations found in leukemic cells. But mutations alone have never fully explained why AML behaves so differently from patient to patient. A new study published in Nature now provides the missing layer: the epigenome.
In the largest chromatin‑profiling effort ever conducted for any cancer, a research team led by Seishi Ogawa, MD, PhD, and Yotaro Ochi, MD, PhD, of Kyoto University, together with Sören Lehmann, MD, PhD, of the Karolinska Institute, mapped the chromatin accessibility landscape of 1,563 AML patient samples. Their analysis—built on ATAC‑seq, RNA‑seq, DNA methylation, ChIP‑seq, whole‑genome sequencing, and single‑cell multiomics—reveals that AML can be classified into 16 distinct epigenomic subgroups, each defined by a characteristic chromatin state and its own regulatory wiring.
As the authors wrote, “ATAC-seq…show[s] that AML can be classified into 16 subgroups on the basis of chromatin accessibility profiles.” This chromatin‑based structure was remarkably stable: single‑cell ATAC‑seq across more than 280,000 cells confirmed that each patient’s leukemic population shares a conserved accessibility fingerprint.
Each subgroup carries a unique combination of driver mutations, differentiation states, transcription‑factor networks, DNA methylation patterns, and super‑enhancer architecture. Many do not align cleanly with existing genomic classifications such as WHO or ICC, according to the researchers. In fact, the team found that even exhaustive decision‑tree analyses of known driver mutations could not explain most subgroup identities. As the paper noted, “Evidence suggests that genetic alterations do not fully explain AML pathophysiology and heterogeneity.”
Clinically, chromatin information sharpened prognostic assessment in both Swedish and Japanese cohorts. Several subgroups also showed unexpected drug sensitivities. Three subgroups responded to MEK inhibitors despite lacking RAS‑pathway mutations. Another subgroup, enriched for RUNX1 mutations and marked by a chromatin profile resembling early B‑cell precursors, proved highly sensitive to ABL inhibitors.
The study, “Chromatin landscape and epigenetic heterogeneity of acute myeloid leukemia,” positions chromatin architecture as a foundational dimension of AML biology. It also provides a practical path toward clinical adoption: the team distilled a 30‑gene expression signature capable of identifying high‑risk chromatin subgroups using standard sequencing workflows.
Looking ahead, the group aims to develop lower‑cost diagnostic approaches and refine treatment strategies tailored to each epigenomic subgroup. The newly generated eCHROMA AML atlas is expected to serve as a resource for cancer epigenomics broadly, enabling discovery of new therapeutic targets and mechanistic insights.
The post Epigenomic Analysis Uncovers New AML Subgroups and Drug Sensitivities appeared first on GEN – Genetic Engineering and Biotechnology News.
A landmark Phase I/II clinical study led by researchers at Skåne University Hospital and Lund University has shown that transplanting stem-cell-derived dopamine progenitor cells into the brain is feasible. Eight patients with Parkinson’s disease (PD) received transplants of STEM-PD, a cryopreserved, off-the-shelf dopaminergic progenitor product derived from human pluripotent stem cells. The three-year Phase I/II, open-label, multicenter, single-arm, dose-escalation study identified no serious side effects linked to the transplanted cells during the first year of follow‑up.
“The possibility of replacing dopamine neurons that are lost in Parkinson’s disease has been a long-standing goal in the field,” said Malin Parmar, professor of cellular neuroscience at Lund University, and lead of the STEM-PD program. “The findings represent an important milestone for regenerative medicine approaches in Parkinson’s disease and support continued clinical development of stem cell-based therapies.”
Results from the study were reported by Parmar and colleagues in Nature Medicine. In their paper, titled “Human embryonic stem cell-derived dopaminergic cells for Parkinson’s disease: a Phase I/II open-label trial,” the team wrote, “In conclusion, particularly in the context of other recently published trials using human PS cell-derived dopaminergic cell therapies for PD, these findings further support the continued development of this therapeutic approach, including evaluation of the STEM-PD product in larger patient cohorts.”
Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease, the authors wrote. In Parkinson’s disease, patients lose nerve cells in the brain that produce dopamine, which leads to symptoms such as slowness of movement, stiffness, gait disturbance, and tremor. “The hallmark pathology of PD involves progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the subsequent loss of their projections to the striatum,” the team explained. Current treatments are medications that replace the lost dopamine, but over time these medications often become less effective and cause side effects.
“Intracerebral transplantation of stem cell-derived dopaminergic progenitors to replace lost endogenous dopaminergic neurons offers a new potentially restorative therapeutic approach for PD,” the investigators continued. Scientists have been working to develop standardized and scalable dopamine cell therapy products derived from pluripotent stem (PS) cells, including human embryonic stem (ES) cells and induced PS (iPS) cells, they noted. “Several such products are now in clinical development … with early safety and feasibility data emerging.”
The transplanted stem cell-based dopamine nerve cell product tested in the newly reported trial is designed to replace the cells that produce dopamine, and the goal is that after being transplanted, the transplanted cells will mature into new dopamine-producing nerve cells in the brain. The STEM-PD trial aimed to evaluate the safety, tolerability, and feasibility of intraputaminal transplantation of STEM-PD in patients with moderately advanced PD.
Eight individuals with Parkinson’s disease received the transplanted cell product at two different doses, followed by 12 months of immunosuppression to prevent graft rejection. All patients were treated at Skåne University Hospital. Seven participants completed 12-month follow-up, and one participant died from a pulmonary infection that was not directly related to the cell product.
The surgical procedure was generally well tolerated, and no graft-induced involuntary movements were observed in the transplanted participants. Clinically, patients remained stable. Imaging using dopamine PET scans provided early indications of graft survival at both 6 and 12 months post-transplantation. Six of the seven participants substantially reduced their dopaminergic medication, a result that will be evaluated over time. In their paper, the team wrote in summary, “This Phase I/II clinical trial involving the bilateral intraputaminal transplantation of the STEM-PD dopaminergic progenitor cell product demonstrates its feasibility with no unexpected safety concerns from the cell product.”
Roger Barker, MD, professor of clinical neuroscience at the University of Cambridge, clinical lead of STEM-PD and clinical PI at the U.K. site, said: “This represents an exciting new departure on repairing the brain of individuals with Parkinson’s using dopamine cells- an approach pioneered in Lund some 40 years ago using fetal dopamine cells. The STEM-PD trial harnessing the expertise of scientists and clinicians from Lund and Cambridge has enabled us to undertake and deliver on one of the first ever stem cell-derived dopamine cell therapies for patients with Parkinson’s, and we hope this will be the beginning of an exciting new programme that may ultimately benefit the wider Parkinson’s community.”
Gesine Paul-Visse, MD, professor in neuropsychiatric research and lead PI at Skåne University Hospital, said, “Reaching this primary endpoint and being able to show that the cell product is safe is a great achievement for this trial, our team, the participating patients, but also for all patients suffering from Parkinson’s disease. We are hopeful that the early signs of cell survival and clinical improvement we observe will continue to increase over time and are excited to continue the development of this cell therapy.”
The STEM-PD research team will now continue the long-term follow-up of the participants to further evaluate safety, graft function, and clinical benefit. “Secondary and exploratory outcomes will evaluate the course and efficacy of clinical features, the survival of grafted dopaminergic cells at 36 months as well as additional safety signals occurring between 12 and 36 months and any dose–response effects,” the investigators stated. “Further evaluation of the grafts up to 36 months will determine whether the implanted cells continue to grow, mature and reinnervate the putamen after 12 months.”
STEM-PD builds on decades of research in dopamine cell replacement therapy for PD at Lund University and pioneering work in translation of pluripotent stem cell technology from experimental studies into clinical evaluation. The STEM-PD trial is the first pluripotent stem cell trial approved in Sweden and the first for PD in Europe. “The initiation and execution of this clinical trial have only been possible through close collaboration between scientists, clinicians, GMP manufacturing teams, regulatory experts and, most importantly, the participating patients,” concluded Parmar. In their report, the authors stated, “The STEM-PD trial adds further important confirmatory and complementary evidence to the recently reported feasibility and short-term safety of PS cell-derived dopaminergic progenitor transplantation in PD.”
The academic Phase I/IIa trial was conducted in collaboration with Novo Nordisk. Cellular Intelligence, a Boston-based company, recently acquired the STEM-PD program and will lead its next phase of clinical development, including a planned Phase II trial. The STEM-PD cells and their continued development hold IND clearance with FDA Fast Track Designation, and Cellular Intelligence aims to advance the program through Phase III to market approval.
STEM-PD is an academic European clinical translation initiative, focused on developing stem cell-based therapies for Parkinson’s disease. The program is led from Lund University with partners from Skåne University Hospital, Cambridge University Hospital, and University College London and combines expertise in stem cell biology, GMP manufacturing, neurosurgery, clinical neurology, and regenerative medicine to advance pluripotent stem cell-derived dopamine neuron therapies toward clinical application.
The post Stem Cell Therapy Shows Promise in First Human Parkinson’s Disease Trial appeared first on GEN – Genetic Engineering and Biotechnology News.