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Alzheimer's disease (AD) is a severe neurodegenerative disease for which there is currently no effective prevention or treatment. The prediction that the number of U.S. patients with AD will triple to approximately 14 million over the next 50 years underscores the urgent need to explore novel...
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by overproduction of β -amyloid (A β ), which is formed from amyloid precursor protein (APP), with the subsequent pathologic deposition of A β in regions of the brain important for memory and cognition. Recently,...
Postmortem analysis of brains of patients with Alzheimer's disease (AD) has led to diverse theories about the causes of the pathology, suggesting that this complex disease involves multiple physiological changes. In an effort to better understand the variety and integration of these changes, we...
Alzheimer's disease (AD) represents the fourth leading cause of death in the U.S. and the leading cause of dementia in the elderly population. Until recently, there was little hope of finding a way to prevent the underlying brain pathology from progressing toward the inevitable conclusion of the...
There have been several reports on the use of β -amyloid (A β ) vaccination in different mouse models of Alzheimer's disease (AD) and its effects on pathology and cognitive function. In this report, the histopathologic findings in the APP+PS1 doubly transgenic mouse were compared after three,...
Although the pathogenesis of Alzheimer's disease (AD) is not fully understood, growing evidence indicates that the deposition of β -amyloid (A β ) and the local reactions of various cell types to this protein play major roles in the development of the disease. Immunization with the A β 1-42...
Pathologic examination in Alzheimer's disease (AD) shows a significant correlation between β -amyloid peptide (A β P) deposition and the clinical severity of dementia. Formation of β -amyloid (A β ) is a complex kinetic and thermodynamic process, dependent on peptide–peptide interactions...
Long-term vaccinations with human β -amyloid peptide 1-42 (A β 1-42) have recently been shown to prevent or markedly reduce A β deposition in the PDAPP transgenic model of Alzheimer's disease (AD). Using a similar protocol to vaccinate 7.5-month-old APP (Tg2576) and APP+PS1 transgenic mice...
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