Mitochondrial dysfunction may play an important role in the pathogenesis of ageing and age-neurodegenerative diseases such as Alzheimer's disease (AD). Platelet mitochondrial membrane potential (reflected by measurement of JC-1 fluorescence ratio) and adenosine 5′-triphosphate (ATP) contents of 24 moderate probable AD patients, 20 age-matched control subjects and 20 young control subjects were measured. Also, a beta-amyloid peptide (Aβ)-induced damage model of platelets was established. After the addition of Aβ, platelet JC-1 fluorescence ratio and ATP content of platelets were measured in 16 AD patients, 20 aged and 20 young control subjects. Young control subjects had higher JC-1 fluorescence ratio than both AD patients and aged control subjects. No significant differences in platelet ATP contents were found among AD patients, aged and young control subjects. After the addition of Aβ, platelet JC-1 fluorescence ratio and ATP content of aged and young control subjects lowered markedly, but no obvious decrease of platelet JC-1 fluorescence ratio of AD patients was found compared with those of aged and young control subjects. Decrease of platelet JC-1 fluorescence ratio of aged control subjects was lower than that of young control subjects following the addition of Aβ. These results indicated that mitochondrial dysfunction may occur during ageing and platelet mitochondria of AD patients and aged subjects showed a tolerance to Aβ-induced damage. Therefore, blood platelets might serve as a biomarker for detection of mitochondrial function and age-related disease.