Tag: Sexual drive and regulation

Posted on

Brain Astrocytes Form Far-Reaching Connections in Mice

A study in mice headed by NYU Langone Health researchers has found that cells long thought to play a secondary role in brain function build their own far-reaching connections. These pathways appear to connect distant regions in ways that had not been mapped before.

Experts usually describe the brain as a network of nerve cells (neurons) that send each other signals to pass along information. These neurons are maintained by another kind of brain cell, the star-shaped astrocyte, which ferries in nutrients and carries away waste.

The newly reported study, headed by Melissa Cooper, PhD, a postdoctoral fellow in the department of neuroscience at NYU Grossman School of Medicine, revealed that, like neurons, astrocytes form organized webs, which enable them to communicate with other specific astrocytes across the brain rather than only sending local, generalized signals. In some cases, the pathways were found to link areas that were not already joined together by neurons.

“For more than a century, neuroscientists have thought of neurons as the main actors in the brain,” said Cooper. “Yet our findings suggest that astrocytes, which are usually viewed as merely support cells, are also running their own widespread signaling pathway, adding another layer to how brain regions stay connected.” The team suggests that while their study was carried out in mice, not humans, the findings form the basis for future studies investigating how astrocyte networks might link with injury, disease, or aging and to learning and memory.”

Cooper is first and co-corresponding author of the team’s published work in Nature, titled “Astrocytes connect specific brain regions through plastic networks,” in which the researchers stated, “Astrocyte networks can directly link brain regions that are not connected by neurons, suggesting that previously unassociated brain regions communicate with one another through gap junction-coupled astrocytes.”

“Neuronal axons have traditionally been considered to be the primary mediators of functional connectivity among brain regions,” the authors wrote, and the role of communication mediated by astrocytes has been largely underappreciated. “This communication occurs through gap junctions—membrane channels that connect the cytoplasm of neighboring cells, enabling them to redistribute resources and share biochemical signals,” the team continued. “Studies using mice lacking astrocyte gap junctions have shown that these gap junctions are necessary for memory formation, synaptic plasticity, coordination of neuronal signaling, and closing the visual and motor critical periods.”

In earlier work, Cooper reported that in a mouse model of the visual neurodegenerative disease glaucoma, astrocytes can redistribute resources from astrocytes around healthy neurons to damaged neurons. Yet the team had no way to see whether this kind of support-cell network extended across the entire brain.

Cooper said the newly reported study is the first to map active, brain-wide communication networks built by astrocytes and to show that these pathways are highly specific. The research relied on a custom-built tracing tool that let the team follow the cells’ connections in far greater detail than had been possible using past methods. “Despite the importance of astrocyte gap junctional networks, studying them has been challenging,” the investigators noted. “Current methods such as slice electrophysiology disrupt network connectivity and introduce artefacts due to tissue damage.”

For their study, the researchers used a harmless virus to deliver “network tracers” into astrocytes in selected brain regions of lab mice. These tracers tagged small molecules as the molecules passed through the gap junctions linking one astrocyte to another, allowing the team to see which cells were part of the same signaling pathway.

The scientists then made the mice’s brains transparent and used a specialized microscope to capture three-dimensional images of every tagged astrocyte. By doing this across hundreds of mice, they could map astrocyte webs across brain areas. “These networks selectively connect specific regions, rather than diffusing indiscriminately, and vary in size and organization,” they reported. “We observe local networks that are confined to single brain regions and long-range networks that robustly interconnect multiple regions across hemispheres, often exhibiting patterns distinct from known neuronal networks.”

A 3D network of interconnected astrocytes imaged inside a whole, transparent mouse brain. Each astrocyte's color shows its distance from the viewer; closer astrocytes are blue, while more distant astrocytes are red. [Cooper et al. Astrocytes connect specific brain regions through plastic networks. Nature. 2026. doi:10.1038/s41586-026-10426-6.]
A 3D network of interconnected astrocytes imaged inside a whole, transparent mouse brain. Each astrocyte’s color shows its distance from the viewer; closer astrocytes are blue, while more distant astrocytes are red. [Cooper et al. Astrocytes connect specific brain regions through plastic networks. Nature. 2026. doi:10.1038/s41586-026-10426-6.]

The tracing tool and brain-clearing method were designed to be relatively low-cost and easy to reproduce so that other labs could use them to study the networks in many brain diseases.

In another part of the study, the team assessed mice that were genetically engineered with astrocytes that lacked gap junctions. The communication networks largely disappeared, suggesting that the pathways are active and depend on these physical bridges.

“By challenging our understanding of how the brain communicates over long distances, our results may offer fresh insight into how it develops, ages, and behaves in conditions such as Alzheimer’s and Parkinson’s diseases,” said study co-senior author Shane A. Liddelow, PhD, an associate professor in the neuroscience and ophthalmology departments at NYU Grossman School of Medicine.

Another key finding was that astrocyte networks are dynamic. When the team trimmed whiskers on one side of the mice’s faces—“this manipulation is known to induce robust structural remodeling in neurons,” the team noted—a pathway from the region that processes whisker touch got smaller and reconnected to different astrocyte partners.

“The fact that astrocyte networks shrink and reroute after a loss of sensory signals suggests they may be shaped by experience,” said study co-senior author Moses V. Chao, PhD, a professor in the cell biology, neuroscience, and psychiatry departments at NYU Grossman School of Medicine. “It also raises the possibility that each of us has a somewhat unique pattern of connections molded by what our brains have learned and lived through.”

The authors plan to investigate which molecules move through the networks and to apply their tracing tool to models of brain disorders. They also hope to examine how these webs change during development and aging, said Chao.

Liddelow emphasized that while gap junctions and astrocytes exist in humans, it remains unknown whether the networks link the same regions in the same way as in mice. Nevertheless, in their paper, the team concluded that their findings “… establish foundation for future exploration of how astrocyte network structure and function are shaped by injury, disease, development, aging and experience-dependent processes such as learning and memory.”

The post Brain Astrocytes Form Far-Reaching Connections in Mice appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on
<![CDATA[Learn how antipsychotics and stress raise prolactin, what symptoms to spot, and when to test—plus practical options to lower levels.]]>
Posted on

Blood-Based Biomarkers, Inflammation, and Co-Pathologies Emerge as Key Themes at AD/PD

The mood at the recent 2026 AD/PD International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders in Copenhagen was notably different from the mood that has hung over much of neurodegeneration research for the past decade.

There was still plenty of caution, and plenty of unanswered questions, and certainly no shortage of technical nuance. But there was also something more concrete than hope: a growing sense that the field now has enough tools, biological insight, and clinical momentum to start probing more deeply and stratifying pathologies of neurodegenerative diseases in patients, at varying stages of progression.

That shift was visible across the meeting. It was there in conversations about co-pathologies, the increasingly central role of inflammation and the rapid maturation of blood-based biomarkers. It also featured in the way industry and academia alike talked about therapy: not as a search for a single silver bullet, but as a move toward combination treatment strategies more familiar from the fields of oncology, cardiology, and other complex chronic diseases.

Henrik Zetterberg, PhD, Gothenburg University

Henrik Zetterberg, PhD, Gothenburg University, University College London, and a guest professor at University of Wisconsin-Madison, one of the field’s most influential biomarker researchers, put the central theme plainly: “I think disease heterogeneity will be the mantra in the coming years, to dissect the molecular underpinnings of this heterogeneity.”

Heterogeneity moves from caveat to core concept

Zetterberg described how biomarker-enabled phenotyping is exposing just how different patient trajectories can be once amyloid begins to accumulate. Some people decline quickly. Others remain resilient for a decade or longer. Some cases that appear clinically similar may in fact be driven by very different molecular constellations.

Geoff Kerchner, MD, PhD, vice president, global head of neurodegeneration at Roche

Geoff Kerchner, MD, PhD, vice president, global head of neurodegeneration at Roche, made a similar point from the therapeutic side. In Alzheimer’s disease, he said, some features remain strikingly consistent across patients.

But once one moves beyond core pathology, “the rate at which that happens varies from person to person,” and that variance is shaped in part by co-pathologies, including alpha-synuclein, TDP-43, and vascular disease.

Steve Williams, MD, PhD, chief scientific officer at Alamar Biosciences, pushed the same logic further, arguing that mixed biology is not the exception but the rule. “Everyone with neurodegeneration is carrying around some combination of other pathologies,” he said. “It’s almost inevitable because it’s a feature of aging.”

Steve Williams, MD, PhD, chief scientific officer at Alamar Biosciences

That view has major consequences. It means the field is increasingly moving away from asking whether a patient is amyloid-positive or tau-positive in a binary sense and toward asking what additional pathological burden may be present, what that burden means for progression, and how it should influence treatment choice.

Betty M. Tijms, PhD, head of science Alzheimer Center Amsterdam

Betty M. Tijms, PhD, head of science Alzheimer Center Amsterdam at Amsterdam UMC, offered a useful example from discovery research. In her work integrating CSF proteomics and lipidomics, she described signals that shift depending on tau status and amyloid background. At one point, she noted that these patterns “will inform which type of patients may require their own, personalized therapies.” It captures the direction of travel: from broad molecular mapping to biologically meaningful subtyping.

Inflammation is no longer a side story

Andréa Lessa Benedet, PhD, University of Gothenburg

Andréa Lessa Benedet, PhD, University of Gothenburg, discussed findings showing that people with faster progression in tau-related pathology had “higher expression of many inflammatory markers in plasma and in CSF.” That observation alone is not enough to settle the longstanding question of whether inflammation is driving disease, responding to it, or doing both. But it adds to a growing body of work suggesting that immune biology is closely tied to the pace of progression.

What made Benedet’s description especially interesting was that the signal was not identical across biofluids. The proteins elevated in CSF were not the same as those elevated in plasma. Yet when her group mapped those proteins to cell types and pathways, the two compartments converged on similar biology. In other words, the field may not always be looking for one-to-one molecular matches between brain-adjacent and peripheral compartments. It may instead be learning to recognize pathway-level concordance.

Benedet pointed to evidence suggesting that amyloid pathology together with inflammation may influence how tau spreads through the brain. That “bit of both” view—driver and response, cause and consequence—may be unsatisfying if one wants a simple mechanism. It may also be closer to biological reality.

The therapeutic implication is obvious. If inflammatory processes help define faster-progressing biology, then they are not merely descriptive. They become candidates for stratification and, eventually, intervention.

Blood-based biomarkers as research infrastructure

Jacob Vogel, PhD, Lund University and SciLifeLab

Few topics drew more sustained attention in Copenhagen than blood-based biomarkers. Kerchner called blood-based biomarkers one of the biggest themes of the meeting saying they could “really democratize the diagnosis of Alzheimer’s disease.”

Democratization here is about health equity—geography, trial access, earlier identification, and the possibility of shifting neurodegeneration research beyond the relatively narrow populations that have historically been easiest to recruit and deeply phenotype. That broader perspective surfaced in a session on sex differences in neurodegeneration, where Jacob Vogel, PhD, assistant professor at Lund University and SciLifeLab, presented findings suggesting that brain cells responding to Alzheimer’s pathology have different expression patterns in men and women. Seen that way, the field needs tools that are sophisticated enough to capture the true biological complexity of disease across different patients.

Niranjan Bose, PhD, managing director, Gates Ventures

However, one excellent blood-based biomarker, such as brain-derived p-tau217, does not solve the co-pathology problem. As Niranjan Bose, PhD, managing director at Gates Ventures put it, there is a growing “need to do better when it comes to co-pathologies so we can stratify participants better.” A strong single analyte may be enough to identify one core process very well; it is not enough to capture the layered biology of aging brains. That is why the discussion is shifting from singleplex to multiplex, from favorite markers to models.

Zetterberg spoke about the new NULISA Neuro 220 panel from Alamar Biosciences, as a research tool that can help the field probe lysosomal and synaptic biology, alpha-synuclein-related processes, and other pathways relevant to co-pathology. He also highlighted the importance of brain-derived tau readouts, arguing that they may reduce confounding from peripheral tau expression and make blood results easier to interpret in diseases where peripheral neuropathy or other non-CNS biology could muddy the picture.

Zetterberg said, “Those broader panels will be the engines for discovery.” In other words, the value of broad biomarker panels is not that every protein measured will someday be run routinely in a clinical lab. It is that broad panels can reveal reproducible patterns, identify hub biology, and narrow the search toward robust clinical assays.

Combination treatment is becoming the default future

The conference’s other major shift was therapeutically focused. Even where amyloid remained central, the discussion increasingly assumed that amyloid-directed therapy alone will not be the endpoint.

Michael Irizarry, MD, senior vice president and deputy chief clinical officer at Eisai US

Michael Irizarry, MD, senior vice president and deputy chief clinical officer at Eisai US, put it bluntly: “Alzheimer’s is being used as the example of precision medicine.” That is a striking statement, because for years Alzheimer’s was more often framed as the place where precision medicine had failed to arrive. What changed is that biomarkers, imaging, and fluid measures have advanced enough to stage disease more accurately and begin matching interventions to biology and timing.

Irizarry also described an emerging combination logic already being tested clinically. “The hope is that by targeting multiple processes we can get a greater treatment effect,” he said, referring to efforts to combine anti-amyloid therapy with a tau-directed antibody strategy. The reasoning is straightforward: if amyloid clearance slows disease but does not stop it, then other mechanisms—including tau propagation—remain actionable targets.

Kerchner made the same point in even broader terms. “The combination of therapies attacking different aspects of Alzheimer’s disease and Parkinson’s disease is almost surely going to be needed,” he said. He compared the situation to hypertension, diabetes, and cardiovascular disease—complex chronic illnesses that are almost never controlled with one intervention alone.

If the field is moving toward a wider therapeutic lens, with multiple mechanisms and intervention points in play, then there is value in creating space for a broader range of emerging approaches. That was visible in the Startup Hub, now in its second year, where early-stage companies gave short five-minute pitches that often echoed the meeting’s main scientific themes. ScandBio was one example: its Phase III clinical trial of a combined metabolic drug targeting mitochondrial dysfunction in Alzheimer’s disease connected to the conference session on mitochondrial pathways in neurodegeneration and therapy.

Taken together, these developments pointed to the same conclusion: as the biology becomes more layered, the response from the field is becoming more layered too. Combination therapy only becomes rational if disease heterogeneity is measurable. It only becomes practical if blood-based biomarkers can help define stage, likely response, and co-pathology burden without requiring every patient to undergo repeated PET imaging. And it only becomes truly precise if inflammation, synaptic injury, lysosomal dysfunction, vascular change, can be integrated into the treatment model rather than treated as background noise.

The post Blood-Based Biomarkers, Inflammation, and Co-Pathologies Emerge as Key Themes at AD/PD appeared first on Inside Precision Medicine.

Posted on

A narrative review on oxytocin at the intersection of sleep, stress, and social behavior

Sleep, stress regulation, and circadian rhythms form an interdependent network that shapes cognition, emotion, and social behavior. Disruption of any component can amplify stress sensitivity and impair emotional regulation, leading to neurobehavioral instability. This review discusses evidence from human and animal studies to illustrate how oxytocin (OT) may function at multiple brain regions to modulate sleep regulation, stress physiology, and social interaction. We discuss mechanisms by which sleep deficiency heightens hypothalamic–pituitary–adrenal (HPA) axis activity and stress-related behavioral reactivity and impulsivity, and how OT signaling is thought to counteract these effects by reducing HPA output and stress-induced behavioral responses. Furthermore, converging evidence from preclinical and emerging human studies suggests that OT release may contribute to non-rapid eye movement (NREM) and rapid eye movement (REM) sleep stability potentially via modulation of hippocampal-amygdalar circuits and thalamocortical network activity, including sleep spindle-related dynamics, thereby enhancing emotional processing and social memory. Social isolation, a potent stressor, reduces OT signaling and disrupts sleep–wake dynamics, suggesting a mechanistic link between positive social interaction and sleep maintenance. Collectively, we propose OT as a key neuromodulatory regulator at the intersection of sleep, stress resilience, and social behavior, providing new insights into the neuroendocrine pathways that underlie adaptive emotional regulation and identifying potential therapeutic targets for stress-related sleep disturbances.
Posted on

Distinct Nature of Parkinson’s Disease Gut Microbiome Identified

Research led by University College London has characterized a specific gut microbiome signature found in people with Parkinson’s disease.

Writing in Nature Medicine, the researchers also found that people carrying a genetic mutation in the GBA1 gene that put them at risk of developing Parkinson’s disease had gut microbiomes similar to people with the condition.

Parkinson’s is the second most common neurodegenerative disease in the U.S. after Alzheimer’s disease affecting more than one million people across the country. By the time full-blown motor symptoms emerge, a large degree of neurological damage has already occurred, so much work is underway to find ways to predict and diagnose early disease, as well as to develop more effective treatments.

“In recent years there has been a growing recognition of the links between Parkinson’s disease—a brain disorder—and gut health,” said co-lead author Anthony Schapira, MD, a professor at UCL Queen Square Institute of Neurology, in a press statement.

“Here we have strengthened that evidence and shown that microbes in the gut can reveal signs of Parkinson’s and may be an early warning signal… years before symptom onset.”

For this study, the researchers evaluated gut microbiome samples from 271 Parkinson’s disease patients, 43 people carrying GBA1 risk variants who did not yet have disease symptoms and 150 healthy controls. They also validated their findings in a further 638 people with Parkinson’s and 319 healthy controls from the U.K., Korea, and Turkey.

Schapira and team used DNA sequencing to see which bacterial species were present in each person’s gut. Comparing people with Parkinson’s disease to healthy controls, they found 176 bacterial species that were more or less common in people with the condition.

For example, people with Parkinson’s had more potentially pro‑inflammatory bacteria, including Bifidobacterium longum and B. dentium, Streptococcus mutans, and Lactobacillus paragasseri, than healthy controls.

In contrast, healthy controls had more helpful, butyrate‑producing gut bacteria from including Roseburia intestinalis, R. inulinivorans and some Faecalibacterium species and less pro-inflammatory species.

Notably, people in the at-risk group who carried a GBA1 risk variant had a gut microbiome somewhere between healthy controls and people with Parkinson’s, suggesting that the composition of microbes in the gut may change over time as the disease develops. In this group, 142 of the 176 species that differed in people with Parkinson’s versus healthy controls also showed changed abundance.

“For the first time we identify bacteria in the gut of people with Parkinson’s that can also be found in those with a genetic risk for the disease, but before they develop symptoms. Importantly, these same changes can be found in a small proportion of the general population that may put them at increased risk for Parkinson’s,” said Schapira.

“This discovery opens the way not only to see if the bacteria are a way to identify those at risk of Parkinson’s, but also to see if changing the bacterial population, through dietary changes or medication, can reduce a person’s risk for Parkinson’s.”

The post Distinct Nature of Parkinson’s Disease Gut Microbiome Identified appeared first on Inside Precision Medicine.

Posted on

AACR 2026: David Parkinson and the Arc of Modern Cancer Therapy

SAN DIEGO, CA – In 1977, when David R. Parkinson, MD, graduated from medical school at the University of Toronto and moved to McGill University to train in internal medicine and eventually hematology, the idea of medical oncology was in its infancy. In Canada, the profession didn’t exist.

“In Canada, there were no medical oncologists,” Parkinson told Inside Precision Medicine. “Radiation therapists administered what little chemotherapy existed. They resisted the development of medical oncology as a specialty.”

David Parkinson - AACR
David R. Parkinson, MD, recipient of the 2026 AACR Outstanding Achievement Award for Service to Cancer Science and Medicine [The American Association for Cancer Research (AACR)]

Through the ensuing 49 years, Parkinson didn’t just see the rise of kinase inhibitors, antibodies, and cell therapies in real-time—he helped create the world of modern cancer therapeutics.

In reflecting on his remarkable career, which was recognized with the 2026 AACR Outstanding Achievement Award for Service to Cancer Science and Medicine, Parkinson said, “I’ve essentially grown alongside the field.”

From scarcity to structure: Oncology’s early years

When Parkinson arrived in Montreal, there were only a handful of chemotherapeutics available. “In those days, there were only one or two drugs available for hematologic malignancies across the entire field,” Parkinson said. “The main treatments were cyclophosphamide and nitrosoureas.”

Even supportive care lagged. “Initially, we had no effective way to control chemotherapy-induced nausea,” he noted of the standard of care for testicular cancer. “Some patients stopped treatment because they couldn’t tolerate it.”

Parkinson explained that early cancer drugs worked best on rapidly dividing tumors, like leukemias and testicular cancers, because that’s what the animal models represented. These therapies targeted DNA and cell division broadly, often with severe toxicity, and were far less effective against slower-growing solid tumors.

After his residency at McGill, Parkinson moved to Boston, first to Tufts New England Medical Center on a modest Canadian fellowship that placed him at the edge of a field just beginning to coalesce. “I was on a Canadian fellowship earning $12,000 a year,” he said. “The exchange rate fluctuated significantly, which made things difficult, and I couldn’t work due to my student visa.”

What he found, however, was momentum. Through connections with Dana-Farber, Parkinson entered formal training in medical oncology as the specialty began to take shape. “I connected with Dana-Farber and took their introductory course for fellows—that was my entry into medical oncology.”

At the same time, breakthroughs in specific cancers hinted at what might be possible. “What really shaped my thinking was the emergence of treatments for testicular cancer just as I entered oncology,” he said. “Platinum-based therapies—and later combination regimens—felt like miracles. We had never seen anything like it. These were often young patients, difficult to manage, but suddenly there were real cures.”

Targeted therapy and the Gleevec moment

Parkinson’s career soon intersected with early efforts to harness the immune system against cancer—decades before immunotherapy became a dominant paradigm. “I became deeply involved in immunotherapy, particularly interleukin-2 and early tumor-infiltrating lymphocyte studies,” he said.

Working at the National Cancer Institute (NCI), he collaborated with leaders, including immunotherapy pioneer Steven Rosenberg, MD, PhD, maintaining a hybrid role that combined research with clinical care. “At the same time, I continued clinical work for a couple of months each year, collaborating with Steve Rosenberg in the surgical branch.”

These early approaches were technically challenging and often unpredictable, but they laid the groundwork for later advances. “We started with basic approaches, moved to tumor-infiltrating lymphocytes, and eventually to engineered CAR T cells,” Parkinson said. “Progress has been steady, though often slower than those treating patients would like.”

If immunotherapy represented one trajectory, targeted therapy represented another—one that depended on a deeper understanding of cancer biology.

“When I joined Novartis in the late 1980s, we were among the first developing kinase inhibitors,” Parkinson said. At the time, the idea was controversial. “Early skepticism suggested kinase inhibitors wouldn’t work due to high intracellular ATP levels and structural challenges.”

But advances in molecular biology were beginning to change the landscape. The discovery of the Philadelphia chromosome and its associated oncogene created a clear therapeutic target. “The Philadelphia chromosome had been known since the 1960s, and by the 1980s the responsible gene was identified,” Parkinson explained.

The result was imatinib (Gleevec), a drug that would become a prototype for precision oncology. “Eventually, a small molecule inhibitor was developed that targeted it precisely.”

The clinical results were extraordinary. “By the third cohort in a Phase I trial, patients with chronic myelogenous leukemia showed dramatic responses—some within 24 hours,” Parkinson said. “It’s probably the only Phase I oncology trial where essentially every patient achieved remission.”

For Parkinson, the implications extended far beyond a single drug. “Of course, [Gleevec] was a unique case,” he said. “But it proved an important point: what once seemed impossible can become possible.”

Since then, the field has expanded dramatically. Hundreds of kinase inhibitors have been developed, with thousands more explored, reflecting a broader shift toward therapies grounded in specific molecular mechanisms.

Precision medicine—and its limits

As oncology evolved, so too did its language. “For years, we called it ‘personalized medicine,’” Parkinson said. “I used to joke that medicine has always been personalized—you’re always trying to determine what’s best for a specific patient in a specific context.”

He credits industry with popularizing a more precise term. “Although Pfizer popularized the term ‘precision medicine,’ I think it’s a better term,” he added, with a note of humor: “I have a few good Pfizer jokes—best shared over a drink.”

Yet the reality of precision medicine has proven more complex than its promise. “The evolution of therapeutics mirrored the models and biological understanding available,” Parkinson said. “Targeted therapies only emerged once we understood the biology. Diagnostics, however, lagged by about two decades.”

That lag remains a structural challenge. Parkinson founded a diagnostics company based on single-cell signaling technology developed at Stanford. “Technically, it worked—we solved major challenges in instrumentation, standardization, and analysis,” he said. “But we couldn’t establish a viable business model.”

The core issue was reimbursement. “Without adequate reimbursement from Medicare, even highly sophisticated diagnostics struggle commercially,” said Parkinson. “Better diagnostics can reduce the use of expensive drugs by identifying who won’t benefit—something that doesn’t always align with pharmaceutical business models.”

In recent years, Parkinson has focused increasingly on large-scale data integration, including his involvement with the GENIE consortium. The initiative aggregates genomic and clinical data across institutions, aiming to accelerate discovery and improve clinical decision-making. “GENIE has been a technical success,” he said. “But its long-term sustainability remains uncertain.”

The broader challenge, he argues, is conceptual as much as technical. “Looking forward, the field is evolving toward integrating multiple data types—genomics, transcriptomics, imaging, and more—to better understand tumor biology,” he said. “Sequencing alone isn’t enough. The challenge now is not a lack of data, but making sense of it—something where artificial intelligence will play an increasingly important role.”

Back to basics

Across academia, government, and industry—including roles at the NCI, Novartis, Amgen, and Biogen Idec—Parkinson sees a single throughline. “I remember an interview with a biotech company where an HR representative told me, ‘You seem to have done a lot of different things,’” he said. “I responded that I had really only done one thing: trying to improve cancer treatment, just from many different angles.”

Not every effort succeeded. “In one case, we developed a drug that performed beautifully in mice but failed in human trials,” he said. “That’s common in oncology—most ideas don’t translate. You don’t think of it as failure but as learning. Still, there’s a limit to how many ‘learnings’ one can appreciate.”

Reflecting on decades of progress, Parkinson emphasizes both how far the field has come and how much remains unresolved. “Outcomes have improved dramatically across several cancers, especially hematologic ones,” he said.

Yet he underscores a fundamental principle: that progress in cancer treatment comes down to understanding biology. “The better we understand it, the more effectively we can develop targeted therapies,” said Parkinson. “Without that understanding, we’re essentially guessing.”

At AACR 2026, Parkinson’s recognition underscores not just past achievements but a continuing trajectory—one shaped by the interplay of discovery, failure, and persistence. “Despite all the challenges,” he said, “[precision medicine] is still the most promising path forward.”

 

The post AACR 2026: David Parkinson and the Arc of Modern Cancer Therapy appeared first on Inside Precision Medicine.

Posted on

STAT+: FDA eyes expanding testosterone therapy for libido

Want to stay on top of the science and politics driving biotech today? Sign up to get our biotech newsletter in your inbox.

Hellooooo, friends. Psychedelics and testosterone are front and center today, but also we note that GLP-1’s dominance in obesity may not be as inevitable as it looks. Early animal data from GLP-1 pioneers suggest that pathways like GIP-glucagon offer effectiveness and better overall tolerability. 

The need-to-know this morning

  • Kailera Therapeutics raised $625 million in an initial public offering — the largest-ever Wall Street debut for a drug company. Kailera is developing obesity drugs licensed from China. 

Do we even need GLP-1 anymore? 

The scientists whose work helped spur the development of GLP-1-based obesity drugs are now questioning whether that target is necessary at all. Instead, they’re proposing that using GIP-glucagon as a dual target could deliver comparable — or even superior — weight loss, without the nausea and dosing limitations that come with current therapies.

Continue to STAT+ to read the full story…

Posted on

Brain Gene Variations Help Explain Neurological and Psychiatric Sex Differences

Thousands of genes are expressed differently in the brains of men and women, researchers have discovered.

The findings could help explain differences in neurodevelopmental, psychiatric, and neurodegenerative disorders between the sexes.

While men are more likely to experience schizophrenia, attention deficit hyperactivity disorder, and Parkinson’s disease, women are more prone to mood disorders and Alzheimer’s disease.

The U.S. study, in Science, is the first systemic single-cell survey of sex differences in gene expression across multiple regions of the human brain.

“Together, these findings provide a comprehensive map of molecular sex differences in the human brain and offer initial insight into their underlying mechanisms and potential functional consequences,” Alex DeCasien, PhD, from the National Institute of Mental Health in Bethesda, Maryland, told Inside Precision Medicine.

DeCasien and co-workers conducted a high-resolution analysis of gene expression in tissue samples from the brains of 15 men and 15 women using single-nucleus RNA sequencing.

They then used data from earlier large neuroimaging studies to select six cortical regions to sample, four of which showed sex-related differences in grey matter volume and two in which no such differences were found.

The team found subtle but widespread differences in gene activity between men and women. Biological sex explained very little of the variance in gene expression across the brain, at less than 1%, but differences were widespread—with more than 3000 genes showing different expression according to sex in at least one cortical region.

The greatest sex-related differences in gene expression were on the sex chromosomes. However, most of the genes showing sex-related variations in expression were autosomal—carried on one of the 22 numbered non-sex chromosomes.

The predominant driver for sex-biased expression of genes on these autosomal chromosomes were sex steroid hormones such as estrogen and testosterone.

Surprisingly, more than half the X chromosome genes in women were expressed in both alleles for at least one cell type. This indicated that many had escaped X chromosome inactivation—a female phenomenon in which one of the two X chromosomes is switched off early in development to stop women producing double the number of X-linked gene products to men.

“That finding has implications for understanding sex-biased disease susceptibility because several genes implicated in neurodevelopmental disorders reside on the X chromosome,” commented Jessica Tollkuhn, PhD, from Cold Spring Harbor Laboratory, and S Marc Breedlove, from Michigan State University, in an accompanying Perspective article.

They noted that autosomal genes showing sex-biased expression were substantially enriched for extracellular matrix components, hormone signaling pathways, and metabolic processes. “Genes with greater expression in women were enriched for mitochondrial and synaptic functions, whereas male-biased genes were associated with metabolic and structural pathways,” the editorialists added.

“By pinpointing these sexually differentiated processes, the data provide a treasure trove for the discovery of biomarkers of and/or therapeutic targets for differential disease risk in men and women.”

DeCasien and team added: “These findings raise the possibility that sex differences in gene expression modulate the magnitude of genetic effects at risk loci, contributing to differences in disease vulnerability and to reduced portability of polygenic risk prediction across sexes.”

The post Brain Gene Variations Help Explain Neurological and Psychiatric Sex Differences appeared first on Inside Precision Medicine.