Triflusal in cerebral vascular disease and in dementia: mode of action

J. García-Rafanell DOI: https://doi.org/10.33588/rn.27S1.98447

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Volumen 27 | Number S1 | Nº of views of the article 5.370 | Nº of PDF downloads 197 | Article publication date 01/12/1998

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ABSTRACT

INTRODUCTION Vascular dementia and Alzheimer’s disease are conditions with a non-well established and probably multifactorial etiology. DEVELOPMENT. Recent studies have suggested that certain antiplatelet agents could be useful in slowing the cognitive impairment of these diseases, not as a consequence of their antiplatelet activity but due to the inhibition of underlying inflammatory processes that contribute to the progression of the disease. Triflusal is a platelet aggregation inhibitor, structurally related to salicylates, with a specific pharmacological and biochemical profile and low hemorrhagic risk. Preliminary data have shown the action of triflusal in the inflammatory mechanisms involved in dementia: 1. It inhibits the activation of the transcription factor NF-kB; this factor regulates the expression of many genes an participates in the processes of neuronal plasticity; 2. It inhibits the expression of cyclooxygenase type-2 (COX-2); recent studies show that this enzyme may be directly involved in neuronal death; 3. It inhibits the expression of the adhesion proteins VCAM-1 and Eselectin, whose participation in the processes of atherogenesis and of endothelial dysfunction and inflammation has been demonstrated. CONCLUSION. The results show the potential interest of triflusal in the prophylaxis of the cognitive impairment in dementia KeywordsCyclooxygenase type-2 Dementia Transcription factor NF-kB CategoriesDemencia Neurodegeneración Neuropsicología Neuropsiquiatría Patología vascular

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Triflusal in cerebral vascular disease and in dementia: mode of action