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Alzheimer's disease (AD) distresses the lives of millions of people around the world. Its costs were estimated to be at least l 00 billion dollars each year (Fill it, 2000). And so far, no cure has been found to stop or slow the progression of the disease. Senile plaques and neurofibrillary tangles are considered to be central in the pathogenesis of AD. The plaques are mainly composed of aggregations of amyloid p (AB) peptides, which are generated upon the sequential cleavage of the larger amyloid precursor protein (APP) first by the enzyme P-secretase, and then by the enzyme y-secretase. These plaques are one of the main targets being explored for newer therapeutic interventions in AD. The transcription factor specificity protein 1 (Sp 1) is associated with the pathology of AD, as it was found to be involved in the transcription of APP and beta site APP cleaving enzyme l (BACE 1) (Christensen et al., 2004, Basha et al., 2005, Santpere et al., 2006). Tolfenamic acid is an NSAID that was reported to lower Sp 1 levels (Abdelrahim et al. , 2006). Accordingly, this study was designed to examine the capability of tolfenamic acid to decrease the levels of the transcription factor Sp 1, and therefore, other AD involved proteins and peptides like APP and AB within animals' brains. Consequently, the drug was administered to C57BL/6 mice and Hartley guinea pigs. Different doses of the drug were tried to find the dosage range where efficacy is achieved. Animals also were sacrificed at different time points, in order to study the drug effects over the time course of the study. Data showed that tolfenamic acid was able to lower SP l, APP and AP in the brains of animal models in a time dependent manner, and within certain doses. These studies demonstrate that tolfenamic acid 1s a potential candidate for further development as a treatment for AD.

Tolfenamic Acid Interrupts the De Novo Synthesis of Plaque-Forming Amyloid Beta Peptides: Implications for Alzheimers Disease