In many recent studies relationship between Alzheimer’s disease (AD) and lipid metabolism is studied. Common denominators of these studies are cholesterol, apolipoprotein E, beta-amyloid (Aβ) and statins. All relationships are not known yet, but the knowledge increases very quickly. It is indisputable, that cholesterol plays an important role at AD. Higher serum levels of cholesterol seem to stimulate beta-secretase, which acts on amyloid precursor protein (APP) and arises Aβ. Cholesterol also facilitates deposition of Aβ into plaques, that are important for development of AD. Cholesterol inhibits alpha-secretase and hence hinders production of neuroprotective solubile APP (APPs). By decreasing removement of cholesterol from brain cells (at polymorphism in the cholesterol-24-hydroxylase gene) the amount of Aβ was increased. Other studies showed, that a certain amount of cholesterol is important for cell membranes to protect them from Aβ. Relationship between AD and apolipoproteinem E (ApoE) ε4 has also been described. This association could be explained by connection of ApoE and higher amount of cholesterol (in blood and brain), which is related to plaques formation. On the other hand, it has been published, that ApoE ε4 supports fibrilogenesis of Aβ regardles on the amount of formed Aβ. It is important to attend to the issue of lipid metabolism disturbance in prevention and therapy of AD in the future.

        Key words: Alzheimer’s disease, cholesterol, apolipoprotein E, beta-amyloid.