Alzheimer's dementia (AD) and vascular dementia (VD) are the two major forms of dementia in the elderly. They have been separated categorically on the basis of pathophysiological findings and clinical operationalized criteria. However, this strict separation has to be reevaluated in the light of recent data. The risk to develop a neurodegenerative dementia in old age is determined by various susceptibility genes and correlated with aging. In AD, the current understanding of pathophysiology focuses on the amyloid cascade hypothesis as the major endpoint of the complex cellular pathology. In VD, incomplete microangiopathic infarcts due to fibrohyalinosis are regarded as the major pathophysiological event. A controversial discussion exists about the coincidence or interaction of genetically determined risk factors of AD and/or VD. Further interactions between AD and VD exist with regard to perivascular mediators and those factors which impair cerebral blood flow. Based on these and other recent neuropathological and therapeutic findings the hypothesis is proposed that the two specific etiopathologies of AD and VD interact to precipitate clinical dementia in the individual and that the individual phenomenology of these dementias is modified by vascular risk factors. Neither, a categorical separation of AD and VD nor the recent idea to regard AD as a distinct form of vascular dementia, do appear convincing.