To date great number of articles were devoted to cholesterol (chol) but only few articles studied the role for chol in neuron function/degeneration. For decades this molecule had been known to be important for atherosclerosis and heart disease. First indication of the involvement of chol in Alzheimer disease (AD), however, come from the mid 1990s. At that time it was shown that heart disease patients develop brain deposits of amyloid beta (Ab or Abeta), a major dogmatic molecule of AD; that apoE (a chol transport apolipoprotein) allele e4 is a major genetic risk factor for AD; and that lab animals fed a chol diet express brain amyloid. These days it turns out that Abeta, long thought to be exclusively a pathologic protein, is a normal and functional apolipoprotein constituent of high density lipoproteins in plasma and CSF. Thus, we and others showed that Abeta modulates chol and phospholipid synthesis, and affects chol esterification. Protection of lipoproteins and other biomolecules from oxidation may represent another important function of Ab. We also discovered that neuronal chol homeostasis failure and the lack of chol supply to neurons by means of lipoprotein transport causes AD features, such as the failure of the neurotransmission and synaptic plasticity, degeneration of neuronal cell processes, and tau protein pathology.