J. Steven Jacobsen Pages 343 - 352 ( 10 )
Alzheimers Disease (AD) is a progressive neurodegenerative disease that is prevalent among the elderly. It is a heterogeneous disease involving a number of genetic components, risk factors and other poorly defined elements that all impact on the accumulation of beta-amyloid peptide (Aβ). Current understanding of pathology, biochemistry and genetics strengthens the notion that Aβ is potentially the common pathogenic agent in an apparent convergence of various mechanisms leading to the decline of cognitive function and neuronal loss. While many issues remain controversial, recent evidence attributing Aβ accumulation to cognitive decline in humans, coupled to the demonstrated improvement of cognitive function following Aβ immunization in pre-clinical models, strongly supports the ”amyloid hypothesis“ and a central role for Aβ in the pathophysiology and etiology of AD. These and other observations endorse the notion that therapeutic strategies targeting the inhibition of Aβ accumulation by the use of protease inhibitors, immunization or other strategies, may provide disease-altering interventions to the development and progression of AD. The only approved and marketed treatments currently available for AD are the acetylcholinesterase inhibitors, a palliative strategy aimed at the temporary improvement of cognitive function. The purpose of this overview is to provide a brief understanding of key events leading to the progression of AD and to highlight a few of the current and most promising therapeutic strategies that one day might be available for the treatment of AD.
neurodegenerative disease, beta-amyloid (a-beta), alzheimers disease, acetylcholinesterase inhibitors a chels, memantine, neotrofin, phenserine, app protease, anti-inflammatory drugs, cholesterol inhibitors
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