Effects of beta-amyloid peptide and estrogen on platelet mitochondrial function of Sprague-Dawley rats

Beta-amyloid peptide (Abeta) peptides play a central role in the development of Alzheimer's disease. They are known to induce mitochondrial dysfunction and caspase activation, resulting in apoptosis of neuronal cells. In the present experiment, an Abeta-induced damage model of platelets was established to observe the effects of Abeta, estradiol benzoate (EB) and genistein on platelets and platelet mitochondria. It was found that after the addition of Abeta, platelet number, platelet mitochondrial membrane potential (DeltaPsim) and adenosine triphosphate (ATP) content were lowered while no protective effects of EB and genistein had been observed. The platelets could serve as a biomarker for detection of mitochondrial function and age related disease.