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Microglia respond to Alzheimer's disease (AD) with varied transcriptional responses. We show that oligomeric Aß (oAß) induces the expression of Hif1a and Egln3 in microglia in vitro, together with the transcription of the type I interferon signature (IFNS) genes in a PHD3-dependent manner. We identify FOXO3 as a repressor of IFNS, whose abundance decreases upon PHD3 induction in response to oAß. In vivo, loss of PHD3 correlates with abrogation of the IFNS and activation of the disease-associated...

Tailpipe emissions from road traffic contribute substantially to the burden of fine inhalable particulate matter (PM(2.5)) and deteriorate air quality. Exhaust emission standards, forcing improvements in combustion and exhaust after-treatment technology, considerably decreases combustion-related PM(2.5) emitted by modern cars. A549 cancerous alveolar and BEAS-2B normal bronchial epithelial cells were exposed at the air-liquid interface to the total aerosol or gas phase of either fresh or...

Mitochondrial damage determines cell fate, leading to mitochondrial autophagy or cellular apoptosis in health and disease. The molecular mechanisms and role of the acto-myosin cytoskeleton regulating mitochondrial clearance and membrane remodeling are critical in neurodegenerative disease progression including Alzheimer, but remain unclear. To investigate the potential link between full-length Myosin VI (FL-Myo6) recruitment and exposure of the mitochondria-specific lipid cardiolipin (CL), here...

Imbalanced production and clearance of amyloid-β (Aβ) is a hallmark pathological feature of Alzheimer's disease (AD). While several monoclonal antibodies targeting Aβ have shown reductions in amyloid burden, their impact on cognitive function remains controversial, with the added risk of inflammatory side effects. Dysregulated stimulator of interferon genes (STING) signaling is implicated in neurodegenerative disorders, yet the biological interaction between this pathway and Aβ, as well as their...

As global aging accelerates, the incidence of thyroid diseases, particularly hypothyroidism, is rising in the elderly. The thyroid-stimulating hormone (TSH) levels increase in healthy elderly populations. However, whether the thyroid undergoes cellular senescence and how this relates to thyroid hormone (TH) synthesis remain unclear. To investigate the molecular and functional characteristics of thyroid aging, we performed scRNA-seq on human thyroids from young, middle-aged, and old groups,...

CONCLUSION: Population aging poses challenges to TB control, highlighting the need for targeted strategies for older adults.

The global population of individuals aged 60 years and older now exceeds one billion and continues to grow, underscoring the necessity of addressing cognitive challenges associated with aging. The present study aimed to evaluate the enhancement and suppression of attentional mechanisms, as well as working memory efficiency (WME), across the adult lifespan. Additionally, it examined factors that may moderate these relationships. A total of 194 participants, aged between 20 and 80 years, completed...

Background Mitochondrial integrity and efficiency deteriorate with age and are linked to cellular senescence. Mitochondria are highly responsive to reduced oxygen availability (hypoxia), which for example occurs when exposed to altitude. We hypothesize that mitochondria are involved in the observed health benefits at moderate altitude. Because the experimental evidence on mitochondrial changes at moderate altitude is limited, we also evaluate dose-response associations of oxygen transport and...

CONCLUSION: This multimodal neuroimaging study highlights altered brain functional connectivity and glymphatic dysfunction as potential neural correlates of PSF in middle-aged and older adults. The findings provide novel insights into the complex pathophysiology of PSF in the aging brain, implicating both functional brain networks and the glymphatic system. Further research is warranted to validate these age-specific findings and explore targeted interventions for PSF in older stroke survivors.