Aug 2026· International Journal of Innovative Technologies in Social Science· 0 citations· 24 references
TL;DR
Despite remaining challenges, including safety concerns and the risk of amyloid-related imaging abnormalities, anti-amyloid therapies represent a major advancement in the treatment of Alzheimer's disease and mark a transition toward disease-modifying strategies.
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, neuronal loss, and the accumulation of β-amyloid plaques and tau pathology. For many years, pharmacological treatment has been limited to symptomatic therapies, including acetylcholinesterase inhibitors and memantine, which provide only modest clinical benefits without modifying disease progression. The development of anti-amyloid monoclonal antibodies has introduced the first disease-modifying therapeutic approach targeting the underlying pathology of AD. Agents such as aducanumab, lecanemab, and donanemab reduce cerebral amyloid burden through selective targeting of different forms of β-amyloid. Clinical trials, including CLARITY AD and TRAILBLAZER-ALZ 2, have demonstrated that these therapies can slow cognitive decline in patients with early-stage AD, although their efficacy depends on disease stage and patient selection. Despite remaining challenges, including safety concerns and the risk of amyloid-related imaging abnormalities, anti-amyloid therapies represent a major advancement in the treatment of Alzheimer’s disease and mark a transition toward disease-modifying strategies.
Despite remaining challenges, including safety concerns and the risk of amyloid-related imaging abnormalities, anti-amyloid therapies represent a major advancement in the treatment of Alzheimer's disease and mark a transition toward disease -modifying strategies.
Kacper Jaskulski, Julia Aleksandra Leśniak, Natalia Maria Leśniak et al.· 0 citations
Alzheimer’s disease (AD) is one of the leading neurodegenerative disorders affecting over 55 million
individuals worldwide, with a limited selection of disease-modifying therapies. The amyloid cascade
hypothesis proposes that amyloid-beta (Aβ) peptide accumulation initiates a cascade of synaptic
dysfunction, neuroinfla...
Rhea Menon· American Journal of Student...· 0 citations
Alzheimer’s Disease (AD) is a neurodegenerative disorder with
progressive cognitive decline, β-amyloid plaques, neurofibrillary tangles, oxidative stress,
and neuroinflammatory responses. So far, the pathogenesis of AD has been explained by
the cholinergic hypothesis, amyloid cascade hypothesis, and tau protein dys...
Lalit Parihar, A. Singh, Sanjar Alam· Current Pharmacogenomics and...· 0 citations
Preliminary results indicate that nanoparticle-mediated delivery significantly enhances the bioavailability and efficacy of AChE inhibitors compared to conventional delivery methods.
Sushma, Rishab Dubey, Rupa Chaturvedi et al.· Journal of Health Synapse· 0 citations
Alzheimer’s disease (AD) is the leading cause of dementia and a heterogeneous neurodegenerative disorder characterized by amyloid-β (Aβ) and tau pathology, impaired proteostasis, neurovascular dysfunction, maladaptive glial and immune responses, and synaptic dysfunction. Human genetic evidence supports an upstream role...
P. Chmielewski· Cells· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.