Tag: Sexual drive and regulation

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Next Generation Biopharma Innovation

Researchers are digging deeper into biology’s complexity. In preclinical research, the traditional in vivo models are simply not enough to fuel the engine with the relevant translational data needed to progress successfully to the clinic.

As research needs evolve in immunology and immune-oncology—as focus on neuroscience increases and metabolic drugs such as GLP-1-based therapeutics become more prevalent—in vivo model suppliers are being requested to up the game on new platforms. In response, these suppliers are expanding their humanization platforms while developing advanced models that can be used to study complex and overlapping disease biology.

Regulatory factors also affect this market. The continued focus on the reduction of the use of animals by U.S. and European regulatory authorities has further opened the door to new approach methodologies (NAMs). NAMs are not new. Organ-on-chip or microphysiological systems, organoids, and iPSCs have been available for years. Finally, these systems are entering the limelight. Although the NAM market still requires more standardization across platforms, these systems are starting to impact preclinical research.

Building translational engines

The Jackson Laboratory (JAX) recently launched its latest humanized model, the NSG®-SGM3-IL15-MHC I/II DKO (S15-DKO). The S15-DKO represents their latest advancement in generating PBMC-humanized mice, supporting broad engraftment of immune cell subtypes such as CD4+ and CD8+ T cells, CD33+ myeloid cells, and CD16+/CD56+ natural killer (NK) cells. The knockout of the murine MHC Class I/II receptors delays the onset of Graft vs. Host Disease (GvHD).

Profile of the NSG-SGM3-IL15-DKO
S15-DKO model is JAX’s latest advancement in generating PBMC-humanized mice, supporting broad engraftment of immune cell subtypes. The knockout of the murine MHC Class I/II receptors delays the onset of Graft vs. Host Disease (GvHD). [The Jackson Laboratory]

The model also supports the engraftment of rare immune cell subsets, including gd T cells and CD19+/CD38+ B cells that retain the memory state of the donor PBMCs.

Another advanced model for CD34+ hematopoietic stem cell (HSC) humanization, the NSG-FLT3-IL15 mouse generates a cellular-diverse human immune system encompassing myeloid cells, mature NK cells, functional dendritic cells, and T cells.

Both models are available in naïve strains, or off-the-shelf pre-characterized PBMC- and HSC-engraftment, along with full preclinical services tailored to immuno-oncology and autoimmune drug discovery.

“With the FDA’s renewed focus on reducing reliance on non-human primates in biologic development, demand for validated, translational preclinical models has never been higher,” said Luke Dimasi, senior director, JAX.

The genetically humanized FcRn platform and the newly expanded Tg32 hALB mouse address this need. Lacking murine Fcgrt and albumin while expressing their human counterparts, the Tg32 hALB is the first model for studying the pharmacokinetics and pharmacodynamics of human albumin therapeutics, as well as human IgG and Fc-domain-based biologics. Preclinical mAb testing services are available.

“Our offering extends beyond the vivarium,” Dimasi emphasized. JAX’s iPSC repository continues to grow with engineered lines carrying disease-relevant mutations linked to Alzheimer’s, Parkinson’s, ALS, and frontotemporal dementia. In 2025, JAX added HALO-tagged and TET-inducible lines to the collection. The acquisition and integration of the New York Stem Cell Foundation (NYSCF) brings complementary patient-derived iPSCs to the portfolio.

“As the field moves towards new approach methodologies (NAMs), we are evolving alongside it,” Dimasi pointed out. “Our in vivo mouse capabilities give us decades of deeply validated biological context. We are now layering human iPSCs and AI-computational phenotyping on top of that foundation to build a convergent translational engine that no single approach could deliver alone.”

Developing relevant models

According to Jason Rashkow, PhD, product manager for research models, Charles River Laboratories, the company’s comprehensive collection of spontaneously developing rat models spans metabolic disease, diabetes, hypertension, and heart failure, providing strong translational relevance across cardiometabolic indications.

Custom diet preconditioning services allow researchers to tailor disease progression to specific study objectives through strategic model selection and diet design. Standardized preconditioning offerings are planned. “This approach will accelerate study initiation, giving researchers faster access to these metabolic disease models,” said Rashkow.

The increasing prevalence of GLP-1-based therapeutics and next-generation incretin and poly-agonist therapies expanding into cardiometabolic indications such as heart failure with preserved ejection fraction (HFpEF) is accelerating demand for advanced disease models. The combination of established disease models, standardized preconditioning approaches, and custom solutions reflects the complexity of modern metabolic drug development.

In addition, optimization of the generation of CD34+ HSC-humanized mice continues. These models, developed on the severely immunodeficient NCG strain, support research in immuno-oncology, autoimmune disease, vaccine research, and related fields.

As immuno-oncology research needs shift, so does the need for models that enable the study of NK cell-based therapies, tumor microenvironment reprogramming, and cancer vaccines. “Although variant NCG models expressing human cytokines or HLA transgenes begin to meet these needs, transgenes can influence humanization requirements,” Rashkow noted.

To counteract this, the company expanded access to a peripheral blood mononuclear cell (PBMC) engrafted NCG variant strain carrying a double knockout for murine MHC class I and class II, which significantly delays the onset of GvHD, allowing for longer-term studies in the context of mature T cells.

To better support researchers studying HLA-A2-restricted immune responses in vivo, humanization optimization of a NCG variant expressing human HLA-A*02:01 was completed. Further development of the humanization protocols for other variant strains will support next-generation immunotherapy discovery and translational research.

Lastly, the expanded aged C57BL/6 mouse offerings support researchers investigating age-related disease. As a licensed distributor of JAX® Mice to researchers in Europe and Asia, Charles River Europe can now provide aged C57BL/6J mice up to 90 weeks of age. In North America, Charles River offers aged C57BL/6N mice up to 77+ weeks of age.

Improving translational fidelity

“Improved translational fidelity, increased demand for study-ready systems that better align with clinical endpoints, and the need to model complex and overlapping disease biology are driving model development,” related Michael Seiler, PhD, vice president of portfolio management, Taconic Biosciences.

Complex modalities such as checkpoint inhibitors and engineered cell therapies require more complete immune system function and deeper phenotyping. Expansion of the FcResolv® NOG portfolio and huSelect™ services reduces murine immune interference and donor variability. Advanced flow cytometry panels support deeper, standardized

immune profiling.

Animals Alternatives
With the goal of improving translation relevance, Taconic develops in vivo models that reflect complex and overlapping disease biology in immunology, immuno-oncology, neurobiology, and cardiometabolic indications. [Taconic Biosciences]

Planned launches include platforms and models designed to support immuno-oncology, biologics, engineered cell therapies, infectious disease, and autoimmune research, with a focus on more complete and functional human immune system biology. Gene and protein analysis services are available.

In neuroscience, the shift is toward better alignment with clinical disease biology, particularly in Alzheimer’s disease and neuroinflammation, along with increased focus on blood-brain barrier (BBB) biology and CNS delivery. Parkinson’s disease model offerings include aSyn KI/KO, PINK1 KO, and LRRK2 KO rat models.

Future models include BBB-focused platforms such as TFRC and CD98, ARTE10 crosses with BBB models, and neuroimmunology-focused NOG variants, including IL-34 and TREM2-related models.

The rapid growth of obesity therapeutics, including GLP-1 and next-generation incretin approaches, is accelerating demand for more predictive metabolic and liver models in cardiometabolic disease. A range of models are aimed at obesity, MASH, cardiovascular disease, and DMPK applications.

Taconic is expanding its capabilities in transgene characterization, CRISPR off-target analysis, and tiered Custom Model Generation Solutions. The acquisition of TransCure bioServices significantly bolsters support of integrated in vivo study services, particularly in humanized immune system and immuno-oncology research. “We now offer a more seamless, end-to-end solution from model selection through study execution and data generation,” said Seiler.

“We continue to evolve toward integrated solutions rather than standalone models. This includes expanded CMS and CMGS capabilities, humanization-as-a-service, deeper phenotyping and multiomic analysis, and partner-enabled data generation,” Seiler added.

Importantly, the move toward integrating in vivo models with complementary technologies such as organoids, iPSCs, and AI-enabled analysis will influence how models are developed and deployed within research workflows.

Standardizing NAMs

The field is clearly shifting toward ready-to-use biology, producing a strong demand for standardized NAM platforms and services that deliver consistent, high-quality results. To facilitate scientists, MIMETAS continues to develop robust OrganoReady® models and advanced services, including immune-competent and vascularized systems across multiple organs.

“Last year, we strengthened our fee-for-service capabilities and advanced several models to deliver high-quality biology in a consistent, scalable way,” said Paul Vulto, PhD, co-CEO and co-founder, MIMETAS. “We made strong progress in our kidney tubuloid research program, CAR T-related applications, and a BBB model under unidirectional flow.”

The novel human distal nephron-on-chip model in the OrganoPlate® replicates physiologic sodium and water transport using primary human kidney cells. This three-dimensional microfluidic platform, as detailed in Kidney360, serves as a high-throughput tool for functional drug screening and investigating distal nephron physiology and disease.1

A polarized kidney tubuloid in an OrganoPlate chip
A polarized kidney tubuloid in an OrganoPlate chip showcases apical and basolateral access. Immunofluorescence 3D reconstruction demonstrates tubule polarization and barrier formation: blue, DNA; red, acetylated tubulin; and green, Na /KATPase. [MIMETAS]

In addition, a three-dimensional BBB microvasculature model developed on the OrganoPlate Graft 48 UniFlow was evaluated in a recent Fluids Barriers CNS publication. Tri-cultures of endothelial cells, pericytes, and astrocytes were used to demonstrate that this pump-free, unidirectional perfused, three-dimensional BBB model outperformed simpler systems on vascular architecture and barrier function. Its high-throughput nature renders the model suitable for studies of BBB function in health, disease, and therapeutic development.2

This year, the company’s UniFlow technology will be offered for in-lab use, enabling customers to create a stable, perfusable vascularized bed for endothelial tissues. New OrganoServices for gastrointestinal toxicity (GI tox) and drug-induced vascular injury (DIVI), alongside a multi-donor expansion of the OrganoReady Colon Organoid product, are also planned.

A major trend in NAMs is the increased need for standardization and regulatory alignment across the field. With initiatives like IAMPS (Industry Alliance for MicroPhysiological Systems), of which MIMETAS is a founding member, industry innovators will work together to advance regulatory acceptance.

The space is evolving quickly, but Vulto emphasized that their focus remains unchanged: building robust human models that help researchers make better decisions.

Improving organoid access

“Organoids are part of a broader innovation focus to help researchers work with more predictive models, more advanced tools, and more connected workflows across the path from discovery to development,” commented Heather Hargett, PhD, head of cell biology reagents franchise at MilliporeSigma, the U.S. and Canada Life Science business of Merck KGaA, Darmstadt, Germany.

The regulatory landscape is becoming increasingly favorable to NAMs. In March 2026, the FDA issued a draft guidance to establish clear validation principles for NAMs, including organoids and in silico (or AI) models, when submitted in support of drug applications.

Phasing out animal use for research and regulatory purposes is also supported by the European Commission’s Roadmap Towards Phasing Out Animal Testing for Chemical Safety Assessments.

Patient-derived organoids
Patient-derived organoids (PDOs) retain individual genetic and phenotypic characteristics, enabling drug response testing across diverse patient backgrounds and disease subtypes. The image shows immunocytochemical (ICC) characterization of human colon PDOs that are positive for the colon-specific marker CA II (green), nuclei (blue) and actin (red). [MilliporeSigma, the U.S. and Canada Life Science business of Merck KGaA, Darmstadt, Germany

HUB’s advanced organoid capabilities are now being combined with the company’s cell culture expertise, manufacturing scale, global commercial reach, and broad life science portfolio to make organoids a more practical and scalable tool in drug discovery and translational research.

Key priorities include expanding the validated organoid biobank across additional therapeutic areas, tissues, disease states, and patient backgrounds. “Last October, we announced a strategic partnership with Promega Corporation,” said Hargett. “By combining our organoid expertise with Promega’s advanced reporter technology, we aim to enable high-throughput screening that helps researchers identify safer and more effective drug candidates.”

The case of petosemtamab, developed by Merus, is a notable example of the real-world impact of organoid technology. Petosemtamab’s efficacy was tested using HUB organoids. The EGFR x LGR5 bispecific antibody has received FDA Breakthrough Therapy Designation for use in combination with pembrolizumab for first-line treatment of PD-L1-positive recurrent/metastatic head and neck squamous cell carcinoma (HNSCC). A global Phase III trial is ongoing. Recently, Genmab acquired Merus for approximately $8 billion USD.

Adopting organoid technology is a capital efficiency strategy, according to Hargett. Patient-derived organoids retain individual genetic and phenotypic characteristics, enabling drug response testing across diverse patient backgrounds and disease subtypes. Organoids support a “fail fast” approach by identifying non-viable candidates earlier, reducing costly late-stage clinical trial failures, and allowing companies to redirect resources toward the most promising programs.

 

References

  1. Bernardi MDL, Dilmen E, Kurek D et al. A Novel Human Distal Tubuloid-on-a-Chip Model for Investigating Sodium and Water Transport Mechanisms. Kidney360. 2025 Nov 1;6(11):1981-1993. doi: 10.34067/KID.0000000992.
  2. Admiraal J, Emeh PO, Bokkers M et al. Building the blood-brain barrier: a scalable self-assembling 3D model of the brain microvasculature under unidirectional flow. Fluids Barriers CNS. 2026 Jan 23;23(1):29. doi: 10.1186/s12987-026-00765-x.

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Evaluating CNS Anti-inflammatory Therapies with Human Brain Organoids

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Inflammatory pathways involving microglia, astrocytes, and cytokine signaling are widely implicated in disorders including Alzheimer’s disease, Parkinson’s disease, ALS, multiple sclerosis, and traumatic brain injury. Yet despite significant investment in anti-inflammatory therapies, clinical success has remained limited.

A primary reason is that conventional preclinical models do not fully capture the complexity of human neuroimmune biology. Many therapies show encouraging results in animal studies but fail to reproduce those effects in human clinical trials.

These limitations have become increasingly problematic as evidence linking neuroinflammation to disease progression continues to grow. Genome-wide association studies have identified immune-related genes associated with Alzheimer’s disease risk, while imaging and postmortem analyses have demonstrated close relationships between inflammatory activation, synaptic loss, and cognitive decline. Drug developers are therefore pursuing therapies directed at neuroimmune biology using models that lack functional human neuroimmune architecture.

CNS-3D Inflammatory Organoids, recently introduced by 28bio, is an assay-ready immunocompetent 3D brain organoid model incorporating neurons, astrocytes, and microglia to evaluate efficacy of anti-inflammatory drugs by quantifying their ability to reduce inflammatory injury, preserve tissue health, and restore neuronal network activity.

The inclusion of microglia is particularly important because it enables researchers to study inflammatory signaling within a more physiologically relevant cellular environment. Rather than measuring isolated cytokine responses in monoculture, researchers can examine how inflammatory activation propagates across interconnected neural and glial populations and how those changes affect tissue integrity and network behavior.

Data presented recently at the Microphysiological Systems World Summit demonstrated distinct cellular responses following exposure to inflammatory stimuli (Fig. 1) including lipopolysaccharide (LPS) and TNF-α. According to the findings, LPS exposure generated a predominantly microglial inflammatory response, while TNF-α produced stronger astrocytic activation patterns. Cytokine profiling also demonstrated measurable increases in inflammatory mediators following stimulation.

Differential microglial and astrocytic responses to inflammatory insults in CNS-3D Inflammatory Organoids.
Figure 1. Differential microglial and astrocytic responses to inflammatory insults in CNS-3D Inflammatory Organoids. CNS-3D Inflammatory Organoids were treated with vehicle, LPS, or TNF-α and assessed by immunofluorescence staining for Iba1-positive microglia and GFAP-positive astrocytes. LPS induced a pronounced microglial response, whereas TNF-α preferentially increased astrocytic activation, highlighting stimulus-specific inflammatory phenotypes within the 3D CNS organoid model.

These findings are highly relevant for therapeutic development because neuroinflammation is not a single biological process. Disease states may involve different combinations of microglial activation, astrocytic dysfunction, oxidative stress, and neuronal injury. Models capable of distinguishing between these responses provide a more predictive framework for evaluating therapeutic candidates.

CNS-3D Inflammatory Organoids also support integration of functional calcium imaging with cytokine analysis, immunostaining, cytotoxicity assays, and molecular profiling. This approach addresses another persistent challenge in CNS drug development: many inflammatory assays quantify molecular markers without determining whether those changes correspond to preservation or disruption of neuronal function.

As neurodegenerative drug discovery continues to confront translational issues, interest is growing in models capable of reproducing human-specific cellular interactions and functional neuroimmune responses. Human brain organoid models help bridge the gap between preclinical findings and clinical outcomes by providing a more physiologically relevant framework for evaluating anti-inflammatory therapeutics in the CNS.

 

June 2026 28bio QR Code

 

To learn more about CNS-3D Inflammatory Organoids, please visit 28bio.com.

 

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Gut microbiome screens could identify risk of Parkinson’s disease years before symptoms appear

Nature Medicine, Published online: 28 May 2026; doi:10.1038/s41591-026-04458-8

Innovative microbiome analysis revealed a part of the gut microbiome that changes coherently from healthy individuals across those with genetic risk of Parkinson’s disease to patients who are symptomatic. A large range of microbiome alterations within each of the three groups enables identification of individuals at greater risk of developing Parkinson’s disease. A healthy diet was inversely associated with these alterations and might mitigate disease risk.

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Mechanisms of action and advances in application of music therapy in improving cognitive impairment based on the theory of neuroplasticity

As global population aging accelerates, preventing and treating cognitive impairment has become a major public health priority. Music therapy is a safe, well-tolerated non-pharmacological intervention with substantial potential to improve cognitive function. This review synthesizes the neurologic music therapy (NMT) framework, encompassing techniques targeting attention, memory, and executive function, delivered through both active and receptive approaches. Clinical investigations indicate that music therapy may improve cognition and neuropsychiatric symptoms in Alzheimer’s disease (AD), vascular cognitive impairment (VCI), Parkinson’s disease–related cognitive impairment, mild cognitive impairment (MCI), and traumatic brain injury (TBI); however, effects appear to vary by intervention duration and disease stage. This narrative review aims to provide a theoretical foundation and practical guidance for the non-pharmacological intervention of cognitive impairment by collating evidence on the neuroplasticity theoretical foundations, technical systems, and clinical applications of music therapy.
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Women’s Memory Decline Linked to ECM Changes from Brain Estrogen Loss

New research from investigators at Northwestern Medicine, published in Aging Cell, shows that loss of estrogen production in the brain after menopause is associated with changes in the brain’s extracellular matrix (ECM), a structure between brain cells that supports communication and memory. The findings suggest that estrogen decline may alter hippocampal brain environment in ways that contribute to memory impairment and may help explain why nearly two-thirds of all people with Alzheimer’s disease (AD) are women.

“This study tells us that females—but not males—may be uniquely sensitive to loss of brain estrogen at old age, potentially contributing to an increased risk of Alzheimer’s disease,” said senior author Hong Zhao, MD, PhD, a research professor of obstetrics and gynecology in the division of reproductive science in medicine at Northwestern University Feinberg School of Medicine.

The researchers found that estrogen loss, aging, and female sex are closely linked to changes in the ECM in the hippocampus, a brain region central to learning and memory. The ECM is a network of molecules that fills the spaces between neurons and glial cells to support cell communication and function. It makes up nearly 20% of brain volume and is important for memory and brain development.

To date, most research into AD has focused on neurons and glial cells, with less attention paid to the ECM. In the Northwestern study, ECM changes were examined as a central feature of brain biology affected by estrogen loss, the first study of its kind, the researchers noted.

For their research, the investigators use genetically engineered mouse models in which estrogen production was disrupted by removing aromatase, an enzyme required for estrogen synthesis. The enzyme was eliminated either throughout the body or restricted to the brain. The investigators examined young and old male and female mice, allowing comparison of sex-specific and age-related effects. The team assessed, behavior and social function, and also collected data on genome-wide gene expression changes in the hippocampus.

The research also built upon the current understanding of estrogen’s role in brain function. In the brain, estrogen has been associated with memory and mood-related functions.

“We have provided some of the most compelling evidence that estrogen is so important for memory function and other mood functions in the female brain,” said author Serdar Bulun, MD, chair of the department of obstetrics and gynecology at Feinberg and a Northwestern Medicine physician. “This should motivate clinicians to be more aware of the essential role of estrogen for women’s brains, because once memory is gone, it’s gone.”

The findings indicate that loss of brain estrogen may disrupt ECM organization in the hippocampus, which may impair communication between brain cells. Because the ECM provides a structural and signaling environment for neurons, any alterations of the ECM potentially affect processes required for memory formation and maintenance.

Prior research has shown that women with AD may have lower brain estrogen levels than women without AD. Hormone replacement therapy (HRT), created restore estrogen levels, has produced mixed results in clinical studies however.

The investigators noted that understanding how estrogen affects brain structures such as the ECM may help explain variability in HRT outcomes and could serve as a new avenue for developing future treatments. Rather than focusing only on restoring hormone levels, future therapies could address downstream changes in brain architecture.

ECM restoration could represent one such therapeutic approach. If estrogen loss leads to ECM disruption in the hippocampus, then interventions aimed at normalizing ECM structure before memory decline may support brain function in postmenopausal women.

The Northwestern team are continuing their investigation of how estrogen regulates ECM composition and signaling in specific brain regions, and whether these changes directly drive memory impairment. The noted that more research is also needed to determine how ECM-related mechanisms interact with other known AD pathways.

The post Women’s Memory Decline Linked to ECM Changes from Brain Estrogen Loss appeared first on Inside Precision Medicine.

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<![CDATA[The ASCp meeting spotlights a fast-acting psychedelic for postpartum depression, vasopressin-targeting drugs, and ketamine’s promise for Parkinson symptoms.]]>
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STAT+: EU and US advisers split over AstraZeneca breast cancer drug 

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Merck’s bet on an antibody-drug conjugate developed in China has paid off in a major Phase 3 lung cancer study, where sacituzumab tirumotecan paired with Keytruda sharply outperformed Keytruda alone in a subset of lung cancer patients.

Also, the NIH is down another leader, and Sam Altman-backed longevity startup Retro Biosciences raises more funds.

Continue to STAT+ to read the full story…

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STAT+: Pharmalittle: We’re reading about a Parkinson’s drug setback, a Merck lung cancer therapy, and more

And so, another working week will soon draw to a close. Not a moment too soon, yes? This is, you may recall, our treasured signal to daydream about weekend plans. Our agenda is unusually busy thanks to a lengthy to-do list that must be tackled before we walk one of the no-longer-so-short people down the aisle. What else? Hard to keep track, but once the chaos subsides, we hope to settle in for another listening party, where the rotation will likely include this, this, this, this and this. And what about you? Spring is in the air, so perhaps this is time to hike a trail, stroll through a park, or take a long drive to nowhere. You could also plan a summer getaway (book now before those fuel costs rise again) or clear out the perennial clutter. If all this is too much or the weather fails to cooperate, you could simply go into zen mode and plan the rest of your life. Well, whatever you do, have a grand time. But be safe. Enjoy, and see you on Tuesday, since there is a long weekend due to a holiday on this side of the pond. …

Biogen and Denali Therapeutics said Thursday that their experimental therapy for Parkinson’s disease failed to slow the degenerative brain disorder in a randomized trial, dealing a substantial blow to a scientific approach that stoked excitement among advocates and academics, STAT explains. In the study, 648 adults with Parkinson’s were randomized to receive either a placebo or a pill targeting a protein called LRRK2. In 2004, researchers discovered that mutations in the LRRK2 gene can cause a rare, inherited form of Parkinson’s. And in 2018, another group of scientists showed that blocking the protein might actually benefit all patients with the disease. The results are a significant setback to the latter idea.

Earlier this month, Genentech offered countless academics and other researchers up to $125,000 in grants to generate papers about several topics that read like key talking points for a trip to Capitol Hill, STAT reports. The company is seeking “rigorous, independent” work that focuses on the potential consequences of U.S. pricing policies on future innovation, the idea that pharmaceutical discovery is a strategic national asset, and the risks surrounding R&D, according to a request for proposals that came with a June 30 deadline for submissions. Such overtures are hardly new, but this particular solicitation appears notable partly because the company is being very direct about seeking research that is designed to address specific points, rather than solicit topics that may — or may not — dovetail with corporate goals.

Continue to STAT+ to read the full story…

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A federal office of men’s health has never been closer, yet it’s likely still years away

WASHINGTON — Just before he was sworn in as assistant secretary for health at the end of 2025, Admiral Brian Christine — a urologist whose practice treated primarily male patients — talked at an FDA panel on testosterone  about a series of alarming statistics: Male life expectancy is close to seven years shorter than women’s; men have higher mortality rates in 10 of the leading causes of death; and they make up the vast majority of deaths by suicide.

“We have a men’s health crisis in this country. Now we need a national strategy,” he said, in a panel on testosterone replacement. He added that establishing a “parallel track” to women’s health for men at the Department of Human and Health Services was a priority of HHS secretary Robert F. Kennedy Jr., and reiterated the message on the day of his swearing in. 

Read the rest…