Early detection and diagnosis of neurodegenerative diseases has been hampered by the lack of sensitive testing. Real-time quaking induced conversion (RT-QuIC) has been used for the early and sensitive detection of prion-induced neurologic disease, and has more recently been adapted to detect misfolded alpha-synuclein and tau as biomarkers for neurodegenerative disease. Here we use full-length recombinant tau substrates to detect tau seeding activity in Alzheimer's disease and other human tauopathies.
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http://dx.doi.org/10.1080/19336896.2020.1832946 | DOI Listing |
J Alzheimers Dis
January 2025
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, India.
Background: Extracellular signal-regulated kinase 1 (ERK1) belongs to mitogen-activated protein kinases, which are essential for memory formation, cognitive function, and synaptic plasticity. During Alzheimer's disease (AD), ERK1 phosphorylates tau at 15 phosphorylation sites, leading to the formation of neurofibrillary tangles. The overactivation of ERK1 in microglia promotes the release of pro-inflammatory cytokines, which results in neuroinflammation.
View Article and Find Full Text PDFHeliyon
January 2025
Grupo de Investigación en Energías Renovables y Meteorología-GIERMET, Universidad Tecnológica del Chocó, Cra 22 No 18b -10, Quibdó, Colombia.
The corrosion rates of carbon steel and galvanized steel according to the ISO 9223 standard, the effect of pollutant contamination and atmospheric aggressiveness under high rainfall conditions in the Chocó department were studied. Carbon and galvanized steel samples, chloride, and sulfur collectors were exposed in three atmospheric stations in three strategic positions covering the Colombian Pacific: Quibdó, Andagoya and Bahía Solano, for different exposure periods (up to 18 months). The structural-micro characterization of corrosion products was evaluated via X-ray diffraction (XRD), Raman spectroscopy and scanning electron microscopy coupled with energy-dispersive X-ray spectroscopy SEM-EDS.
View Article and Find Full Text PDFMol Neurodegener
January 2025
College of Life Sciences and Oceanography, Brain Disease and Big Data Research Institute, Shenzhen University, Shenzhen, 518060, Guangdong, China.
Background: Astrocytes, the most abundant glial cell type in the brain, will convert into the reactive state in response to proteotoxic stress such as tau accumulation, a characteristic feature of Alzheimer's disease (AD) and other tauopathies. The formation of reactive astrocytes is partially attributed to the disruption of autophagy lysosomal signaling, and inhibiting of some histone deacetylases (HDACs) has been demonstrated to reduce the molecular and functional characteristics of reactive astrocytes. However, the precise role of autophagy lysosomal signaling in astrocytes that regulates tau pathology remains unclear.
View Article and Find Full Text PDFJ Neurochem
January 2025
Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Brain damage induced by ischemia promotes the development of cognitive dysfunction, thus increasing the risk of dementia such as Alzheimer's disease (AD). Studies indicate that cellular acidification-triggered activation of asparagine endopeptidase (AEP) plays a key role in ischemic brain injury, through multiple molecular pathways, including cleavage of its substrates such as SET (inhibitor 2 of PP2A, I ) and Tau. However, whether direct targeting AEP can effectively prevent post-stroke cognitive impairment (PSCI) remains unanswered.
View Article and Find Full Text PDFMolecules
December 2024
Department of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Chiba, Japan.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with cognitive dysfunction, memory decline, and behavioral disturbance, and it is pathologically characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. Although various hypotheses have been proposed to explain the pathogenesis of AD, including the amyloid beta hypothesis, oxidative stress hypothesis, and abnormal phosphorylation of tau proteins, the exact pathogenic mechanisms underlying AD remain largely undefined. Furthermore, effective curative treatments are very limited.
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