Functional APP acts as a chaperone targeting mitochondrial creatine kinase and other proteins from cytoplasm to mitochondria, and this chaperoning role could be disrupted by decreased APP function, resulting in decreased levels of mitochondrial creatine kinase, reduced phospho-creatine and thus increased creatine deposits, which support the statement that an intake of creatine supplementation in AD may be futile, leading to a further increase in creatine deposits without bioenergetic improvement [104]. Here, APP is linked to Alzheimer disease.