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Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) composed of tau aggregates. Research in animal models has generated hypotheses on the underlying mechanisms of the interaction between Aβ and tau pathology. In support of this interaction, results from clinical trials have shown that treatment with anti-Aβ monoclonal antibodies (mAbs) affects tau pathology.
View Article and Find Full Text PDFDrug Development.
Alzheimers Dement
December 2024
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Australia, Melbourne, VIC, Australia.
Background: Iron is vital for metabolism but can act as a catalyst for oxidative damage. Elevated brain iron, determined from biomarkers of iron (CSF ferritin and quantitative susceptibility mapping MRI) and from post-mortem measurement of brain iron, has been associated with accelerated cognitive decline in multiple Alzheimer's disease (AD) clinical, cohorts. These findings supported the hypothesis that treatment with the brain-permeable iron chelator deferiprone may be associated clinical benefit in AD.
View Article and Find Full Text PDFDrug Development.
Alzheimers Dement
December 2024
Kyunghee University Hospital at Gangdong, Seoul, Korea, Republic of (South).
Background: Recent preclinical studies have revealed a significant reduction in amyloid-β plaques and pro-inflammatory cytokines in Alzheimer's disease (AD) mouse models following low-dose radiation therapy (LDRT). This phase II, multicenter, prospective, single-blinded, randomized controlled trial (NCT05635968, funding from Korea Hydro & Nuclear Power: Grant No. A21IP11) aims to investigate the efficacy and safety of whole-brain LDRT in patients with AD.
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 PDFBackground: Lecanemab is an approved anti-amyloid monoclonal antibody that binds with highest affinity to soluble Aβ protofibrils, which are more toxic than monomers or insoluble fibrils/plaque. In clinical studies, biweekly lecanemab treatment demonstrated a slowing of decline in clinical (global, cognitive, functional, and quality of life) outcomes, and reduction in brain amyloid in early Alzheimer's disease (AD). Herein, we describe the impact of lecanemab treatment on tau PET.
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