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Scientists have identified an enzyme that may act as a natural defense against the worsening of fatty liver disease, which affects an estimated 100 million Americans. The enzyme, called UBE2N, helps liver cells clear away damaged mitochondria and break down fat, potentially preventing the inflammation, scarring, and cell damage associated with the more dangerous condition MASH.

The essential amino acid leucine can boost cellular energy production by protecting key proteins on mitochondria from being destroyed. The discovery reveals a new connection between nutrition and metabolism that could eventually lead to new approaches for metabolic disorders and cancer.

Scientists have linked a gut bacterial compound called ImP to greater Alzheimer’s risk, harmful brain protein buildup, and faster cognitive decline. The finding raises the possibility that reducing ImP in the blood could one day help slow or prevent dementia.

Vitamin C may do more than support the immune system. In a phase 2 trial of people with precancerous or low risk blood cancers, daily vitamin C did not slow abnormal cell growth, but it was linked to favorable changes in inflammation and fewer serious complications. An exploratory follow up also found fewer deaths among participants taking vitamin C than among those receiving placebo.

Transcription factor-based direct conversion of somatic cells represents an interesting avenue for generating induced neural stem cells (iNSCs) from peripheral blood without transit through a pluripotent stage. While this paradigm has been shown to be associated with epigenetic de-aging, the dynamics of this process have remained unclear. Here, we used overexpression of the two reprogramming factors SOX2 and cMYC to generate iNSCs from erythroid progenitors of donors ranging from neonatal to 101...

Alzheimer's disease (AD) is associated with amyloid β (Aβ) accumulation, neuronal metabolic dysfunction, and structural degeneration. This study compares the neurotoxic effects of Aβ25-35 and Aβ1-42 in the rat cerebral cortex and hippocampus and evaluates the neuroprotective potential of proline rich peptide 1 (PRP-1). Amyloid peptides were administered bilaterally into the lateral ventricles, followed by intramuscular PRP-1 at 0.1 mg/kg once daily for three weeks, beginning 24 h after amyloid...

CONCLUSION: Repeated plantar electrical stimulation was associated with shortened early SEP latencies elicited by lower-limb nerve stimulation. No comparable latency shortening was observed in median nerve SEPs, suggesting that the observed changes were more prominent in lower-limb than in upper-limb somatosensory processing. These findings suggest that repeated plantar electrical stimulation may be associated with changes in the temporal characteristics of lower-limb somatosensory processing in...

Vulnerability to fraud and financial exploitation among older adults is an increasing public health concern. Growing evidence supports that cognitive and socioemotional changes with age contribute to greater exploitation risk among older adults, while the neural mechanisms of heightened susceptibility to deception in aging are not well understood. Of note, white matter tracts are particularly impacted in aging and are likely implicated in deception detection. This study, for the first time,...

The diaphragm is the primary respiratory muscle. Like other skeletal muscles, it is subject to age-related changes, but it may be more resistant to sarcopenia due to compensatory mechanisms operating at the neuromuscular junction (NMJ). Here, we examined key parameters of neuromuscular transmission in the diaphragm of 24- and 3-month-old mice. In aged NMJs, a decrease in the amplitude of evoked postsynaptic responses in combination with a much greater reduction in miniature end-plate amplitude...

In addition to cell cycle arrest, cellular senescence is characterized by disrupted mitochondrial homeostasis, development of the senescence-associated secretory phenotype (SASP), and alterations in the immune microenvironment. Mitochondrial membrane damage, disrupted mitochondrial dynamics, and impaired mitochondrial quality control (MQC) can occur during cellular senescence. These changes may cause mitochondrial DNA (mtDNA) to leak abnormally into the cytosol. Cytosolic mtDNA can then activate...

Aging represents a major contributor to the deterioration of female fertility, with oocyte quality being the central determinant of ovarian aging, a key factor underlying infertility. Although several natural compounds with anti-aging activity have been documented, highly effective strategies to reverse ovarian aging remain elusive. Here, we report that the peptide elamipretide preserves ovarian function and sustains female fertility during maternal aging. We found that elamipretide...

Nearly 6 in 10 people with high blood pressure in a large England study had never been diagnosed or treated, and half of those already taking medication still had elevated readings. Researchers say a more proactive approach to finding and controlling hypertension could prevent thousands of heart attacks and strokes.

High-risk MDS stem cells appear to have an unexpected “energy addiction,” relying far more heavily than healthy blood-forming cells on a molecule called NAD. Disrupting this energy pathway selectively weakened the cancer-driving cells, revealing a potential new target for treatment.

Cellular senescence has undergone a remarkable conceptual evolution since its discovery in 1961. Initially described by Hayflick and Moorhead as the finite proliferative lifespan of cultured human cells, senescence was first viewed as a consequence of cellular aging. The identification of telomere shortening, senescence biomarkers, and oncogene- and damage-induced senescence subsequently established its molecular basis and role as a tumor-suppressive stress response. The discovery of the...

Twenty years after the discovery of induced pluripotent stem cells, the field has progressed from patient-specific disease modeling toward cell-based therapies for neurodegenerative disorders. Parkinson's disease has emerged as the leading model for neuronal replacement, whereas Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis require distinct combinations of circuit reconstruction, cellular support, immune modulation, and engineered therapeutic delivery. We discuss...

Parkinsons disease, characterized by the aggregation of alpha-synuclein is a complex neurodegenerative disorder with the fastest global prevalence growth. The identification of shared genes expressed in both blood and brain of Parkinson's disease patients improves the knowledge on peripheral pathophysiology of the disease and facilitates identification of minimally invasive potential biomarkers from these shared genes. Our study intends to identify a shared transcriptomic signature between the...

No therapies ensure long-term survival of dopaminergic neurons in Parkinson's disease. In this context, we propose that early neurodegeneration is an adaptive state of transmissive dormancy, not dysfunction. Upon sensing cellular stress, an inducible transcriptional program restricts cytosolic dopamine and actively silences neurotransmission. This adaptive response precedes neuronal death, reframing early symptoms as programmed dormancy rather than frank degeneration. Thus, reactivation...

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Sleep and circadian disturbances are associated with cognitive decline and dementia. Narcolepsy type 1 (NT1), characterized by severe sleep-wake disruption and loss of hypocretin, would therefore be expected to predispose individuals to premature brain aging. Yet available biomarker and neuroimaging findings do not consistently support this possibility, raising questions about the role of hypocretin in mechanisms linking sleep to neurodegeneration. Beyond maintaining wakefulness, hypocretin...

Neurodegenerative disease is marked not just by loss of proteins or cells, but by dynamic rewiring of macromolecular interaction networks that precede and drive pathology. Here, we present a temporally resolved, systems-scale map of multi-protein complex remodeling in a tauopathy model, integrating co-fractionation mass spectrometry, quantitative phosphoproteomics, and machine learning to decode phosphorylation-dependent shifts in protein interactomes across disease progression. This...