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Taking a closer look at immune ‘memory’ could spur progress in the fight against lethal illnesses

The average human has about 1.8 trillion immune cells. These cells patrol the body for bacteria, viruses, cancers, and other threats. Vaccines enhance this security system by teaching our immune cells to target specific pathogens. According to the World Health Organization, vaccine-induced immunity saves about six lives every minute. But how long does this protective immune “memory” last?

According to Shane Crotty, Ph.D., Professor and Chief Scientific Officer at La Jolla Institute for Immunology (LJI), we still have much to learn about immune memory.

“There are actually not many studies of human immune memory due to vaccines,” says Crotty. “Scientists traditionally don’t track immune memory past one year after vaccination—or even six months after vaccination—and that’s a bit of a problem.”

Translational prospectives for deep brain stimulation and low-intensity focused ultrasound neuromodulation: IFCN Handbook chapter

[IFCN Handbook chapter: DBS and focused ultrasound neuromodulation] Neumann & Darmani: “In the present book chapter we review emergent innovations that have recently surfaced or are imminent to make the leap, improving the treatment of patients with brain disorders.”


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MS Risk Upped Significantly With EBV Mononucleosis

Laboratory-confirmed Epstein-Barr virus-positive infectious mononucleosis (EBV-mono) was linked to a more than threefold higher risk for multiple sclerosis (MS) than not having EBV-mono, a new retrospective study showed.

“Mononucleosis is a relatively uncommon illness, but developing strategies to prevent infection with the virus that causes this disease could help us to lower the number of MS cases in the future,” lead study investigator Jennifer L. St. Sauver, PhD, Mayo Clinic, Rochester, Minnesota, said in a press release.


Epstein-Barr virus-positive infectious mononucleosis (EBV-mono) is associated with a threefold higher multiple sclerosis risk than not having EBV-mono, new research shows.

Heart Rate Variability Moderates the Association Between Trait Anxiety and Sympathetic Nerve Activity in Humans

A new study challenges the long-standing view that Alzheimer’s is driven primarily by amyloid plaques, instead pointing to a subtle but critical competition inside neurons.

New research led by the University of California, Riverside, suggests Alzheimer’s disease may not be driven solely by plaque buildup in the brain, as widely believed. Instead, it may result from one protein disrupting the normal function of another.

For years, scientists have focused on amyloid beta (a-beta) as the main cause of Alzheimer’s. Clusters of this protein are commonly found in patients, and genetic mutations that raise a-beta levels are known to trigger early-onset Alzheimer’s.

A stretchy, heat-activated skin patch could be a surgery-free melanoma treatment

FOR IMMEDIATE RELEASE

“A Stretchable, Transparent, Photothermally Stimulated Laser-Induced Graphene Patch for Noninvasive Skin Tumor Treatment” ACS Nano

Melanoma is a deadly form of skin cancer that is typically removed surgically. Now, researchers publishing in ACS Nano report they have developed a potential noninvasive treatment for melanoma in the form of a stretchy, heat-activated patch similar to a bandage. When activated, the patch releases copper ions that kill the underlying cancer cells and prevent them from spreading. In tests with mice, the researchers say the patch reduced melanoma lesions without damaging surrounding tissue.

CRISPR takes a bold leap toward silencing Down syndrome’s extra chromosome

Scientists have taken an important step toward a gene therapy that could one day turn off the extra genetic material that causes Down syndrome (DS). Down syndrome is a genetic condition caused by an extra chromosome 21 (and consequently hundreds of triplicate genes) that leads to developmental and neurological issues. According to the Washington-based National Down Syndrome Society, approximately 1 in every 640 babies in the United States is born with DS. That makes it the most common chromosomal condition.

Traditional gene therapy targets one or two genes, but in this approach, scientists at Beth Israel Deaconess Medical Center and Harvard Medical School found a way to silence much of the extra chromosome’s activity in the cell at once.

Details of their research are published in a paper in the journal Proceedings of the National Academy of Sciences.

Immunogenic XAPs are released by NETosis and associated with high-risk vasculopathy in patients with SSc

AutoimmuneDiseases affect nearly 50 million Americans, and 4 out of 5 patients are women.

https://doi.org/10.1172/JCI198291 In this Research Letter, Howard Y. Chang & team show novel autoantibodies target hotspots on the XIST ribonucleoprotein complex in female-biased autoimmune diseases.


1Department of Dermatology and.

2Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.

3RNA Medicine Program, Stanford University, Stanford, California, USA.

4Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Abstract: In obesity, the heart muscle can thicken, preventing it from relaxing properly between beats

While diet and inflammation likely contribute, the underlying molecular mechanism has been unclear.

https://doi.org/10.1172/JCI196238 Here, Junichi Sadoshima & team find direct stimulation of IL-6 transcription by PPARα in cardiomyocytes plays an important role in mediating the initial development of obesity cardiomyopathy.

The figure indicates binding of PPARα to NFkB (via PLA assay).


1Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, New Jersey, USA.

2Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Address correspondence to: Junichi Sadoshima, Cardiovascular Research Institute, Rutgers Biomedical and Health Science, 185 South Orange Ave., MSB G609, Newark, New Jersey, 7,103, USA. Phone 973.972.8619; Email: [email protected].

Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson’s Disease

💡 by Catanesi, M., et al. (2026). Biomedicines, 14, 313. 📖Read the full text: https://brnw.ch/21x1AQl.

Neurodegenerative diseases continue to challenge modern medicine, with mitochondrial dysfunction emerging as one of their most critical hallmarks. Among the most intriguing recent discoveries is the role of mitochondrial‑localized microRNAs (mito‑miRNAs), small regulatory molecules capable of influencing mitochondrial gene expression and cellular metabolism. As research uncovers their presence and function within the mitochondrial environment, these molecules are gaining attention for their potential involvement in the onset and progression of disorders such as Parkinson’s disease. Understanding how mito‑miRNAs contribute to neuronal vulnerability may open new avenues for diagnostics and therapeutic strategies in neurodegeneration.


Neurodegenerative diseases (NDs) are the most prevalent age-associated disorders, characterized by progressive neuronal loss and cognitive decline. Mitochondrial dysfunction is strictly associated with NDs and represent one of the hallmarks of these disorders, with neurological syndromes frequently representing the primary clinical manifestations of mitochondrial abnormalities. As central regulators of cellular bioenergetics, mitochondria play a pivotal role in both the physiological maintenance and pathogenesis of disease by different regulatory approaches. One of these, microRNAs (miRNAs), a class of small non-coding RNAs, are well-established regulators of gene expression across different biological pathways.

A missing link in how the brain regulates appetite

Bile acids at the center of hepato-ocular crosstalk.

Hepatic dysfunction with ocular pathology has been linked to dysregulated bile acid metabolism.

Bile acid imbalance has been shown to drive ocular injury along the gut-liver-eye axis through direct cytotoxicity, disruption of retinal and lens homeostasis mediated by FXR and TGR5 signaling, and immune activation and these mechanisms are implicated across a spectrum of conditions, ranging from inborn metabolic disorders to acquired cholestatic diseases.

The researchers in this review discuss translational potential of targeting bile acid homeostasis and summarize emerging therapeutic strategies, including bile acid-based interventions, targeted drug delivery, and microbiome modulation, that aim to restore systemic bile acid balance.

Thus, bile acid homeostasis act as a unifying therapeutic framework for hepato-ocular comorbidities. sciencenewshighlights ScienceMission https://sciencemission.com/Hepato-ocular-crosstalk


Health sciences.

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