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Background: Anti-amyloid beta (Aβ) immunotherapies have recently evolved as promising treatment options in patients with early symptomatic Alzheimer's disease (AD). Meanwhile, accurate patient selection for these treatments might be challenging mirrored by strict selection criteria of the hitherto published clinical trials. Based on a real-world tertiary care sample of post-mortem validated cases, we aimed to identify the patients matching these selection criteria and their proportion showing post-mortem AD pathology.

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Alzheimer's disease is the most prevalent form of dementia in the elderly, which is clinically characterized by a gradual and progressive deterioration of cognitive functions. The central and early role of β-amyloid in the pathogenesis of Alzheimer's disease is supported by a plethora of studies including genetic analyses, biomarker research and genome-wide association studies in both familial (early-onset) and sporadic (late-onset) forms of Alzheimer's. Monoclonal antibodies directed against β-amyloid demonstrate slowing of the clinical deterioration of patients with early Alzheimer's disease.

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A cross-sectional analysis of open payments from pharmaceutical companies to memory center physicians.

J Am Geriatr Soc

December 2024

Division of Geriatric Medicine, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Background: The development of anti-amyloid monoclonal antibodies has changed the landscape of care for patients with Alzheimer's disease (AD). The potential for financial conflicts of interest (COIs) for physicians related to these medications is unknown.

Methods: A cross-sectional analysis of open payments from industry to physicians working in memory clinics was conducted.

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Alzheimer's disease (AD), a leading cause of dementia, presents a formidable global health challenge intensified by the aging population. This review encapsulates the evolving landscape of AD diagnosis and treatment with a special focus on the innovative role of fluid biomarkers. Pathologically, AD is marked by amyloid beta (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau, which lead to synaptic dysfunction, neuronal loss, and cognitive decline.

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