Alzheimer's Disease

ALZHEIMER'S DISEASE, named after the author who first described it at the beginning of the current century. This rarely encountered disease begins in old age and is characterized by the slow development of profound mental decay, accompanied by phenomena of organic brain damage. Over a number of years, patients gradually become demented, have difficulty understanding their surroundings, become incapacitated, do not recognize their loved ones, their memory weakens, apathy appears, etc. Subsequently, restlessness develops; patients mutter something to themselves, sing, laugh, and become fussy. At the same time, speech disintegrates: patients pronounce individual words and then only inarticulate sounds; finally, they lose the ability to write, answer questions, become untidy, helpless, and cannot eat independently. General weakness and gait disorders develop, contractures appear, mainly in the legs, as well as asymbolic, paraphasic, and apractic disorders; the reaction of the pupils is sluggish; there are no paralyses or pareses. Ultimately, it reaches an extremely profound physical and mental marasmus; death occurs from incidental diseases or from general exhaustion. Thus, the disease progresses steadily, and the prognosis is extremely unfavorable. Upon microscopic examination, a huge number of amyloid bodies (see) are noted in the cerebral cortex, as well as fatty degeneration of nerve elements and Alzheimer's changes of intracellular fibrils; in place of the perished nerve cells, only piles of pigment and thick, pathologically altered fibrils are visible; glia proliferates, especially around the amyloid bodies. Inflammatory phenomena are not noted; in the vessels, only ordinary arteriosclerotic changes are observed. Pathological-anatomical changes indicate a great similarity of Alzheimer's disease to senile dementia, but all changes in Alzheimer's disease are more intense. An antemortem diagnosis of the disease may present difficulties only in terms of distinguishing it from cerebral arteriosclerosis, to which, however, gross focal symptoms, strokes, etc., are more characteristic, with a less pronounced tendency toward mental decay. It remains unclear whether Alzheimer's disease should be considered merely a variety of senile dementia or an independent disease form. Although anatomical studies point to the first possibility, the fact that Alzheimer's disease develops at a younger age (in the 5th or 6th decade) compared to senile dementia and manifests with much sharper clinical and pathological-anatomical changes speaks for the presence of some unknown factor that determines the specific pathogenesis of this disease.

M. Gurevich. Alzheimer's changes of neurofibrils. Intracellular fibrils change pathologically, stick together, and form thick, strongly staining strands; this change in fibrils is a sign of severe damage to nerve cells, which subsequently disintegrate, after which the altered fibrils, being remnants of nerve elements, continue to stain (persistence). These changes are best seen when stained with the usual methods used to detect fibrils (neurofibrils—Bielschowsky, etc.), but such changes are noticeable even with Nissl staining, which generally does not detect unchanged fibrils. Alzheimer's changes of fibrils are observed in senile dementia and in Alzheimer's disease, being an important distinguishing feature of them.