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Scientists at UC San Diego have unveiled a potentially game-changing treatment for MASH, a severe fatty liver disease affecting millions worldwide. The experimental drug, ION224, blocks a liver enzyme that drives fat buildup and inflammation, two key forces behind liver damage. In clinical trials, patients showed striking improvements in liver health, even without losing weight.

A drug combo widely explored for anti-aging may actually damage the brain, according to new mouse research showing severe loss of myelin and changes linked to “chemo brain.” Surprisingly, the damaged cells resembled those seen in multiple sclerosis, giving scientists a new lead in understanding—and potentially repairing—the disease.

A new experimental treatment could finally offer hope for millions of people with dry age-related macular degeneration — one of the leading causes of blindness in older adults. Researchers at Aalto University discovered a way to gently heat tissue at the back of the eye using near-infrared light, triggering the cells’ natural “cleanup and repair” systems before major damage occurs.

While mitochondria are recognized as promising therapeutic targets for common pathologies of aging, existing drug discovery platforms fail to capture the adequate physiological and biological contexts necessary to identify translatable, clinically-relevant leads. The goal of this study was to identify marine natural products that modulate mitochondrial function using a screening pipeline leveraging primary human cells in a cell-based phenotypic primary screen. Using this approach, we identified...

The anterior cingulate cortex (ACC) is particularly vulnerable to aging, which impairs cognitive functions such as attention and working memory. Although aging is known to alter intrinsic electrophysiological properties in other brain regions, the differences in the properties of aged ACC neurons and young adult neurons remain uninvestigated. In this study, we compared the intrinsic membrane properties and firing characteristics of aged layer 2/3 pyramidal neurons (26-month-old rats) with those...

CONCLUSION: These results show the impact of food insecurity and functional limitations and HRQOL in older adults. The results emphasize the urgent need for addressing food insecurity and promote healthy aging among older adults in New York City.

Researchers found that drinking guava juice may significantly improve anemia by helping the body absorb iron more efficiently. In a review of 17 studies, women and teenage girls who consumed guava juice — especially with iron supplements — experienced noticeable increases in hemoglobin levels. Since guava contains far more vitamin C than oranges, scientists believe it could become a simple, affordable nutrition tool in regions where anemia is widespread.

Vitamin B12 has long been seen as a health hero, helping the body make red blood cells, repair DNA, and keep nerves functioning properly. But scientists are discovering that the story may be more complicated than simply “more is better.” While too little B12 can damage DNA and raise cancer risk, some studies suggest that extremely high levels — especially from long-term high-dose supplements — may also be linked to certain cancers or poorer outcomes in cancer patients.

Scientists in Japan have created powerful new vitamin K-based compounds that may help the brain regenerate lost neurons — a breakthrough that could one day change how diseases like Alzheimer’s and Parkinson’s are treated. By combining vitamin K with components related to vitamin A, the researchers developed compounds that were about three times more effective at turning neural stem cells into neurons than natural vitamin K alone.

Researchers at Texas A&M have developed a nasal spray that appears to reverse brain aging by calming inflammation and restoring the brain’s energy systems. After just two doses, memory and cognitive function improved for months, raising hopes for future treatments targeting dementia and brain fog.

Selective butyrylcholinesterase (BChE) inhibition is gaining renewed attention as a potential therapeutic strategy for Alzheimer's disease (AD), particularly in advanced stages marked by a shift from acetylcholinesterase (AChE) to BChE dominance. Beyond cholinergic regulation, BChE participates in metabolic, inflammatory, and affective pathways, including the enzymatic control of acyl ghrelin that influences appetite, energy balance, and mood. Preclinical and experimental evidence suggests that...

Alzheimer's disease (AD) is a progressive neurodegenerative illness marked by cognitive impairment, synaptic dysfunction and neuronal death. Tau protein abnormalities and mitochondrial dysfunction are key features of its pathogenesis, and both are involved in driving disease development. Emerging evidence suggests that pathogenic tau not only destabilizes microtubules but also directly compromises mitochondrial dynamics, bioenergetics and quality control, ultimately aggravating...

Mitochondrial targeting of the PINK1 kinase results, under normal conditions, in membrane-potential-driven inner membrane penetration and cleavage by the resident protease PARL before retro-translocation and proteasomal degradation. In compromised mitochondria, with reduced membrane potential, inner membrane incorporation is not achieved, which leads to surface activation of the full-length protein, Parkin recruitment and mitophagy. Here, we identify a third pathway in which PINK1 is imported...

Endoplasmic reticulum autophagy (ER-phagy) is a selective autophagy pathway in which receptor proteins target ER membranes and proteins for degradation, yet its role in Alzheimer's disease (AD) remains unclear. Here, we identify FAM134B/RETREG1 as a specific ER-phagy receptor mediating amyloid precursor protein (APP) degradation. FAM134B directly interacts with ER-localized wild-type and familial mutant APP via their C-terminal domains and recruits LC3 through its LC3-interacting region (LIR) to...