[Neuropathologic principles of senile dementia]

Several groups of senile dementias with differing causes and neurohistological substrates can be distinguished. Genetically determined Pick's disease produces severe neuronal atrophy; Alzheimer's disease is characterized by pathological neurofibrillary changes. Jakob-Creutzfeldt disease and Gerstmann-Sträussler-Scheinker disease are slow virus diseases induced by unconventional agents. These diseases, after an incubation time of several years, take the course of slowly progressive degenerative diseases of the central nervous system without inflammatory and specific immune reactions of the host organism. Regarding pathogenesis these diseases were interpreted as degenerative processes as long as their transmissibility was yet unknown. The fact that so-called slow virus diseases can also produce argyrophilic plaques is a further common feature of this group of diseases and human pathological aging processes. So far, however, there is no proof that Alzheimer's disease is caused by an unconventional agent. On the other hand, common features of the products of aging changes and of unconventional viral diseases are apparent. In this paper current knowledge of pathogenetic mechanisms in this rapidly developing field of research is presented. Some relevant factors of organic dementia are discussed: special characteristics of neuronal atrophy (functional role of dendrites); architectonics of cerebral atrophy (laminar versus modular atrophy); neurotransmitter changes (causes or sequels of dementia) and a possibly non-specific origin of senile plaques. Finally, the clinical relevance of neurobiological research into dementias is emphasized.