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Alzheimers Dement
December 2024
Deep Human Biology Learning (DHBL), Eisai Inc., Nutley, NJ, USA.
Background: We developed a highly sensitive immunoassay method using lecanemab that selectively captures amyloid-β (Aβ) protofibril (PF). To characterize Aβ-PF in human cerebrospinal fluid (CSF), we investigated the CSF Aβ-PF levels in patients with Alzheimer's disease (AD) at different disease stages. We also studied the association of CSF Aβ-PF with other AD-related biomarkers.
View Article and Find Full Text PDFBackground: Recent advances in optical clearing and light sheet imaging have opened an exciting new avenue for brain-wide, cellular resolution immunostaining at the forefront of a dimensional shift from 2D to 3D histology. When looking for read-outs of genetic or pharmacological manipulations that affect the entire brain, traditional 2D immunohistochemistry approaches limit observations to brain regions of interest. Providing access to the intricate anatomy of the whole intact brain, tissue clearing offers neuroscientists unbiased and complete views of brain anatomy and function.
View Article and Find Full Text PDFBackground: Microglial activation is one of the neuropathological hallmarks of Alzheimer's disease (AD). Evidence suggest that chronic activation of microglia cause neuroinflammation and neuronal injuries, contributing to cognitive impairment. Therefore, modulation of microglial pathway like CSF-1R represents an attractive therapeutic strategy.
View Article and Find Full Text PDFLecanemab-Associated Amyloid-β Protofibril in Cerebrospinal Fluid Correlates with Biomarkers of Neurodegeneration in Alzheimer's Disease.
Ann Neurol
January 2025
Department of Neurology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Objective: The Clarity AD phase III trial showed that lecanemab reduced amyloid markers in early Alzheimer's disease (AD) and resulted in less decline on measures of cognition and function than placebo. Herein, we aimed to characterize amyloid-β (Aβ) protofibril (PF) captured by lecanemab in human cerebrospinal fluid (CSF) from living participants with different stages in AD, which enable an enhanced understanding of the dynamic changes of lecanemab-associated Aβ-PF (Lec-PF) in vivo.
Methods: We newly developed a unique and highly sensitive immunoassay method using lecanemab that selectively captures Lec-PF.
Residual microglia following short-term PLX5622 treatment in 5xFAD mice exhibit diminished NLRP3 inflammasome and mTOR signaling, and enhanced autophagy.
Aging Cell
November 2024
Institute for Regenerative Medicine, Department of Cell Biology and Genetics, Texas A&M University Health Science Center School of Medicine, College Station, Texas, USA.
While moderately activated microglia in Alzheimer's disease (AD) are pivotal in clearing amyloid beta (Aβ), hyperactivated microglia perpetuate neuroinflammation. Prior investigations reported that the elimination of ~80% of microglia through inhibition of the colony-stimulating factor 1 receptor (CSF1R) during the advanced stage of neuroinflammation in 5xFamilial AD (5xFAD) mice mitigates synapse loss and neurodegeneration. Furthermore, prolonged CSF1R inhibition diminished the development of parenchymal plaques.
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