Search

During the course of Alzheimer's disease, considerable amounts of abnormal proteins accumulate within the brain, in particular in the cortex. Some of this material is extracellular (amyloid), some within the neurons (neurofibrillary changes). The extent of the pathological deposits is variable, some regions being particularly severely involved. The entorhinal cortex is already destroyed in the initial phase, followed, in a stepwise fashion, by the hippocampus and the association areas in the isocortex. The undisturbed transfer of information from the isocortical association areas to the hippocampus via the entorhinal area is of importance for mnestic functions. The destructive cortical changes of Alzheimer's disease lead to early and severe impairment or complete blockage of this information pathways.

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.

In comparison with the silver impregnation methods and with the thioflavine-S fluorescence method astra blue staining is an adequate technique for the demonstration of senile plaque and changes in Alzheimer's fibrils. Astra blue staining proved to be a useful tool in routine tests.

In Wistar rats the intraveneous injection of streptozotocin (65 mg/kg body weight) caused a permanent hyperglycemia. After 5 days there were lesions in the exocrine parenchyme of the pancreas and its nerve fibers. Pathological changes were found in cytoplasm, cell membrane, nucleus and all other cell organelles, too. The zymogen granules remaining after extensive degranulation may disintegrate in two different ways: 1. Shrinking of the granules and formation of a hale between granule membrane and core, the electronic density of which is decreased; indistinct demonstrability of the granule membrane and finally its decomposition. 2. Shrinking of the granules, decrease of the electron density and either homogeneous or mainly peripheral arrangement of the disintegrated material of the granules; irregular shape of the granules and splitting of their membranes.

A method is described, which is based on an impregnation with a silver nitrate solution (pH = 5,0), and on a physical development.

A method based on mordantation with silver nitrate solution at pH = 3.0 and on physical development is described.