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Exploring the Multifaceted Landscape of MASLD: A Comprehensive Synthesis of Recent Studies, from Pathophysiology to Organoids and Beyond

Soft drink consumption is linked to an increased risk of major depressive disorder and greater depressive symptom severity, mediated by changes in gut microbiota, particularly Eggerthella abundance.


Question Is soft drink consumption related to depression diagnosis and severity, and is this association mediated by gut microbiome alteration?

Findings In this cohort study, soft drink consumption was significantly associated with diagnosis of major depressive disorder, as well as depression severity, across a single-study cohort of 932 clinically diagnosed patients and healthy controls. This association was significantly mediated by Eggerthela abundance in female patients and controls.

Meaning Education, prevention strategies, and policies aiming to reduce soft drink consumption are urgently required to mitigate depressive symptoms; in addition, interventions for depression targeting the microbiome composition appear promising.

Study uncovers distinct genetic blueprints for early- and late-onset depression

A new study is providing a clearer picture of the genetic landscape of major depression, revealing that the disorder may have fundamentally different biological roots depending on the age at which it first appears. The research, published in Nature Genetics, found that depression beginning in adolescence or young adulthood has a stronger genetic basis, is linked to early brain development, and carries a much higher genetic association with suicide attempts compared to depression that starts later in life.

Major depressive disorder is recognized as a clinically diverse condition, meaning its symptoms and course can vary substantially from person to person. Researchers have long suspected that this clinical variability might stem from different underlying causes.

One of the most apparent distinctions among individuals with depression is their age at onset. Depression that emerges early in life is often associated with more severe outcomes, including suicidal behavior, while late-onset depression has been linked more frequently to cognitive decline and cardiovascular problems.

One of the world’s oldest blood pressure drugs may also halt aggressive brain tumor growth

A Penn-led team has revealed how hydralazine, one of the world’s oldest blood pressure drugs and a mainstay treatment for preeclampsia, works at the molecular level. In doing so, they made a surprising discovery—it can also halt the growth of aggressive brain tumors.

Over the last 70 years, hydralazine has been an indispensable tool in medicine—a front-line defense against life-threatening , especially during pregnancy. But despite its essential role, a fundamental mystery has persisted: No one knows its “mechanism of action”—essentially how it works at a molecular level, which allows for improved efficacy, safety, and what it can treat.

“Hydralazine is one of the earliest vasodilators ever developed, and it’s still a first-line treatment for preeclampsia—a hypertensive disorder that accounts for 5%–15% of worldwide,” says Kyosuke Shishikura, a physician-scientist at the University of Pennsylvania. “It came from a ‘pre-target’ era of , when researchers relied on what they saw in patients first and only later tried to explain the biology behind it.”

Bridging Retinal and Cerebral Neurodegeneration: A Focus on Crosslinks between Alzheimer–Perusini’s Disease and Retinal Dystrophies

In the early stages of Alzheimer–Perusini’s disease (AD), individuals often experience vision-related issues such as color vision impairment, reduced contrast sensitivity, and visual acuity problems. As the disease progresses, there is a connection with glaucoma and age-related macular degeneration (AMD) leading to retinal cell death. The retina’s involvement suggests a link with the hippocampus, where most AD forms start. A thinning of the retinal nerve fiber layer (RNFL) due to the loss of retinal ganglion cells (RGCs) is seen as a potential AD diagnostic marker using electroretinography (ERG) and optical coherence tomography (OCT). Amyloid beta fragments (Aβ), found in the eye’s vitreous and aqueous humor, are also present in the cerebrospinal fluid (CSF) and accumulate in the retina. Aβ is known to cause tau hyperphosphorylation, leading to its buildup in various retinal layers.

Speaking more than one language may help the brain stay younger

Speaking more than one language can slow down the brain’s aging and lower risks linked to accelerated aging.

In a new study, researchers analyzed the Biobehavioral Age Gap (BAG) —a person’s biological age using health and lifestyle data, then compared it to their actual age—of over 80,000 participants aged 51–90 across 27 European countries. They found that people who speak only one language are twice as likely to experience accelerated aging compared to multilingual individuals.

Researchers suggest that the protective effect might arise from the constant ongoing mental effort required to manage more than one language. The findings of this study are published in Nature Aging.

Exercise-induced vesicles boost neuron growth when transplanted into sedentary mice

Researchers at the University of Illinois Urbana-Champaign report that extracellular vesicles released into the bloodstream during aerobic exercise can, on their own, drive a robust increase in adult hippocampal neurogenesis when transferred into sedentary mice, even without changes in hippocampal vascular coverage.

Aerobic physical activity preserves cognitive function across the lifespan and repeatedly links to structural and cellular plasticity in the hippocampus. Evidence from plasma transfer experiments indicates that bloodborne factors from exercising animals can transfer pro-neurogenic and pro-cognitive effects to sedentary or aged recipients, partly through reduced inflammation.

Many circulating molecules have been implicated in this exercise–brain connection, including , insulin-like growth factor 1, platelet factor 4, selenoprotein P, irisin, cathepsin B, L-lactate, and interleukin-6. Each contributes to specific aspects of neurogenesis or neuronal survival.

Association of Platelet Aggregation With Markers of Alzheimer Disease Pathology in Middle-Aged Participants of the Framingham Heart Study

Background and ObjectivesVascular dysfunction contributes to Alzheimer disease (AD) and related dementias (ADRDs), but the underlying mechanisms remain unclear. Previous studies link midlife hemostasis and platelet aggregation measures to late-life…

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