Abstract
Alzheimer's disease (AD) is the most common type of dementia occurring in mid- to late-life, affecting more than 4 million individuals in United States. The amyloid β—protein (Aβ), which is generated from the amyloid precursor protein (APP) by β- and γ—secretase cleavages, is a major component of pathological plaques that accumulate in AD brains. The majority of AD patients develop the disease due to over–secretion or faulty clearance of Aβ peptide. Thus down–regulation of the expression of Aβ or stimulation of the Aβ clearance process may ameliorate or cure the devastating disease. We are developing gene therapy vectors to favorably alter the metabolic imbalance of Aβ in AD brain. Replication–defective HSV vectors have proven to be attractive vehicles for central nervous system gene therapy because of the natural tropism of the virus for neurons.
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