[Amyloidosis, expression and cause of presenile and senile mental and physical regression. A revision of the amyloid problem (author's transl)]

Abstract

New historic, morphologic, localisatory, chemical, etiological and pathogenetical observations urge the revision of problems of the so-called amyloidosis and suggest a new logical terminology. Cerebral amyloidosis, which corresponds to the clinical picture of senile dementia and Alzheimer's disease, is the local manifestation of a generalized systemic degeneration typified by amyloidotic deposits in aged persons. Chronic lingering tuberculosis, traumatic cerebral injury, genic aberrations, ionising radiations as well as a chronic "slow" virus infection (in cases of Creutzfeldt-Jakob's disease) proved to be inducers of cerebral amyloid deposits. Glenner and his associates succeeded in transforming Bence-Jones albumin into amyloid in vitro. The present writer observed the direct development of amyloid from vascular elastic fibers, from the ground substance of cartilage and osteoid tissue, and from fibrin. Regression of cerebral, cardiac and hepatic amyloid deposits occurs. Similarities between electron microscopic structures bring about difficulties in the morphologic definition of amyloid and cause tinctorial and ultramicroscopic resemblances between cellulose, amyloid and certain vira, although they represent chemically and biologically different materials.