Recent data favor the hypothesis of a genetically-induced overproduction of amyloid protein as the cause of Alzheimer's disease. This could be responsible for the occurrence of senile changes (senile plaques and neurofibrillary tangles) which are both characteristic of so-called normal aging of the brain and of Alzheimer's disease and lead to neuronal death. However, as shown by studies of twins, epigenetic factors must be very important in the triggering and/or acceleration of this process since the concordance between monozygotes does not reach higher levels than 41. It is argued that brain microglia, and/or astrocytes are the most likely candidates to the regulatory function of amyloid deposit in the brain. These cells could act by modulation of either the hydrolysis of the precursor protein during amyloidogenesis or the resorption of amyloid fibrils, which could occur in Alzheimer's disease as suggested by recent data. Further research on this topic could have therapeutical repercussions.