Authors describe 2 cases of likely iatrogenic cerebral amyloid angiopathy after cadaveric dura mater use for cardiac surgery during infancy. Both are remarkable for their early age at onset, lack of genetic risk factor, and demonstration of brain amyloidosis.
To alert on the risk of interhuman transmission of β-amyloid (Aβ) pathology leading to cerebral amyloid angiopathy (CAA) after non-neurosurgical procedures, here cardiovascular procedures, using cadaveric dura mater (DM) patches.
Millions of neurons branch throughout our bodies, keeping them in close communication with our brains. This peripheral network begins to take shape long before birth, as the cells of a growing embryo move into position and adopt their specialized roles. This crucial stage of human development can’t be monitored directly, but by examining genetic clues that linger in adult cells, scientists have now gained surprising insights into the developmental origins of the peripheral nervous system.
Researchers led by Xiaoxu Yang, Ph.D., at University of Utah Health, and Keng Ioi Vong, Ph.D., and Joseph Gleeson, M.D., at the University of California San Diego, have discovered that within the first few weeks of development, some of an embryo’s cells have already been selected to take on particular roles in the peripheral nervous system. Their findings, recently reported in the journal Nature, overturn longstanding assumptions in biology.
Their discovery could change the way scientists think about treatments for a variety of childhood diseases that begin in the cells of the peripheral nervous system.
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.
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.
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Over the years, computer scientists have used cutting-edge processors to simulate the brains of increasingly more complex animals. They’ve already simulated worm and fruit fly brains, and are now working on mice. But according to a new paper, they’ve made a breakthrough that might allow them to simulate human brains, which contain 80 billion neurons compared to a fruit fly’s 140,000. Let’s take a look.
Paper: https://arxiv.org/abs/2512.
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💡 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.
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.
Picture this: your brain is a high-performance engine. Over decades, it doesn’t just wear down, it also starts to run hot. Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.
Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older. Until now.
A landmark study by researchers at Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.