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| http://dx.doi.org/10.1007/s00415-024-12361-w | DOI Listing |
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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Background: The growing number of AD patients is a public concern all over the world. During the decade, anti-amyloid beta-proteins (Aβ) monoclonal antibodies for AD patients have been developed. Among the immunotherapeutic agents, lecanemab is an anti-Aβ monoclonal antibody that binds to Aβ protofibrils (Aβ PFs), which is an intermediate molecule in Aβ species.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia worldwide. The recent announcement that lecanemab, a monoclonal antibody targeting amyloid-b, can slow down cognitive decline in AD is a great step forward in the battle against the disease. However, the modest success achieved in the clinical trial speak to the need for developing additional pharmaceutical approaches to target other key features of AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Eli Lilly and Company, Indianapolis, IN, USA.
Background: Anti-amyloid-β (Aβ) immunotherapy trials have shown amyloid-related imaging abnormalities (ARIA) as the most common and serious adverse events linked to pathological changes in cerebral vasculature. Nevertheless, the mechanisms underlying how amyloid immunotherapy triggers vascular damage, increases vascular permeability, and results in microhemorrhages remains unclear. Notably, activation of perivascular macrophages and infiltration of peripheral immune cells have been implicated in regulating cerebrovascular damage.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brunel University London, London, United Kingdom.
Background: Psychosis occurs in 30-40% of individuals with AD. New insights into disease mechanisms may lead to novel pharmacological targets and treatments. Previous studies have focused on bulk tissue analysis with limited results.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Tel Aviv university, Tel Aviv, Israel, Israel.
Background: Amyloid filaments formation is a complex kinetic and thermodynamic process. The dependence of peptide polymerization on peptide-peptide interactions to form a β-pleated sheet fibrils and the stimulatory influence of other proteins on the reaction suggest that amyloid formation may be subject to modulation METHOD: In vitro formation of β-amyloid was induced by incubation of an aqueous solution of AβP (10 mg/ml) for 7 days at 37°C. The extent of β-amyloid formation and disaggregation were monitored using a panel of well characterized mAbs raised against soluble AβP fragments.
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