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(Circulation Research. 2002;90:1145.)
© 2002 American Heart Association, Inc.

Editorials

Platelets in Atherosclerosis

A New Role for ß-Amyloid Peptide Beyond Alzheimer’s Disease

Alain Tedgui, Ziad Mallat

From INSERM U541 and Institut Fédératif de Recherche - Paris-7, Hôpital Lariboisière, Paris, France.

Correspondence to Alain Tedgui, PhD, INSERM U541, 41, Bd de la Chapelle, 75475 Paris Cedex 10, France. E-mail tedgui@infobiogen.fr

Key Words: platelets • macrophages • ß-amyloid peptide • inflammation

By the mid-1970s, Russell Ross had developed his popular "response to injury" hypothesis of atherogenesis, which postulated that the lesions of atherosclerosis arise as a result of focal injury to arterial endothelium, followed by adherence, aggregation, and release of platelets.^1,2 During the release reaction, platelet-derived growth factor (PDGF) is secreted from the platelets and promotes the proliferative response of smooth muscle cells considered at that time to be the main promoter of atherosclerotic lesion formation. It has since been clearly demonstrated that smooth muscle cell proliferation is a repair process allowing plaque stabilization,³ and that atherosclerosis is a chronic inflammatory disease initiated by monocyte/lymphocyte, but not platelet, adhesion to the endothelium.^4,5 Platelets are therefore unlikely to be involved in the early stages of atherosclerotic plaque formation. Yet, they actively participate in the severe clinical manifestations of atherosclerosis, including sudden death, myocardial infarction, and stroke, which mainly result from atherosclerotic plaque disruption leading to thrombus formation.⁶ In this issue of Circulation Research, De Meyer et al⁷ provide novel insight into the possible role of platelets in plaque inflammation. By using immunohistochemical analysis, this group demonstrates for the first time that both amyloid precursor protein (APP) and ß-amyloid peptide (Aß) are present in advanced human carotid plaques. Up to this time, Aß accumulation in brain tissue has been considered the hallmark of Alzheimer’s disease (AD), a progressive neurodegenerative disease that is prevalent among the elderly. The Aß in AD senile plaques is a metabolite of the APP that forms when an . . . [Full Text of this Article]

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