Results 261 to 270 of about 9,650,018 (348)

TREM2 Drives Neutrophil Extracellular Traps‐Induced Dendritic Cell Maturation and Contributes to Lupus Progression

open access: yesAdvanced Science, EarlyView.
TREM2 recognizes NETs‐derived MPO to promote DC maturation and antigen presentation, thereby exacerbating the autoimmune response in SLE. Mechanistically, TREM2 activation triggers the DAP12/SYK/ERK cascade and enhances NETs internalization by DCs, which in turn activates the cGAS/STING signaling pathway.
Jingxian Shu   +7 more
wiley   +1 more source

Mitochondrial CISD1 Modulates Microglial Metabolic Reprogramming to Drive Stress Susceptibility in Mice

open access: yesAdvanced Science, EarlyView.
CDGSH iron sulfur domain 1 (CISD1) mitigates oxidative stress by promoting NADH oxidation and Coenzyme Q (CoQ) reduction. Under chronic stress, elevated CISD1 expression in microglia enhances NAD⁺ production, thereby increasing GAPDH activity and glycolytic flux, while reducing ATP synthesis by inhibiting proton transfer from mitochondrial complexes I ...
Wanting Dong   +5 more
wiley   +1 more source

The amyloid-beta wave hypothesis of Alzheimer's disease. [PDF]

open access: yesFront Cell Infect Microbiol
Miller SJ, Logan R, Zhang C, Hafler BP.
europepmc   +1 more source

A Robust Serum Proteomic Signature of the E2 Allele of Apolipoprotein E

open access: yesAdvanced Science, EarlyView.
This study expands a serum protein signature of the e2 allele of APOE using multiple proteomic platforms and UK Biobank replication. The signature supports the role of APOE in lipid regulation through apolipoproteins and inflammation and includes, among others, neutrophil secreted granule proteins CAMP, CTSG, DEFA3, and MPO that point to inhibition of ...
Paola Sebastiani   +20 more
wiley   +1 more source

Morphological and Hyperphosphorylation Transitions of Nanoscale Tau Aggregates in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
Super‐resolution microscopy identifies nano‐sized tau aggregates (nano‐aggregates) and reveals distinct transitions in their morphology and phosphorylation profiles across control, Primary Age‐Related Tauopathy, and Alzheimer's disease brains. Morphology and hyperphosphorylation signatures distinguish physiological from pathological forms, with nano ...
Adriana N. Santiago‐Ruiz   +5 more
wiley   +1 more source

TRIM56 Aggravates Cerebral Ischemia‐Reperfusion Injury via Inhibiting KLF4‐Activated Ferroptosis Signaling

open access: yesAdvanced Science, EarlyView.
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang   +15 more
wiley   +1 more source

Segmentation-Guided Development of Visual Classification Criteria for Alzheimer’s Disease

open access: yes
Peters M   +4 more
europepmc   +1 more source

Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease

open access: yes, 2002
S. Seshadri   +7 more
semanticscholar   +1 more source

NAD⁺ Reduction in Glutamatergic Neurons Induces Lipid Catabolism and Neuroinflammation in the Brain via SARM1

open access: yesAdvanced Science, EarlyView.
NAD⁺ homeostasis maintains neuronal integrity through opposing actions of NMNAT2 and SARM1. Loss of NMNAT2 in glutamatergic neurons reprograms cortical metabolism from glucose to lipid catabolism, depletes lipid stores, and triggers inflammation and neurodegeneration.
Zhen‐Xian Niou   +9 more
wiley   +1 more source

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