Senile Plaques

Senile plaques ( syn. neuritic plaques, senile drusen, drusen brain ) are extracellular deposits of beta- amyloid in the gray matter. The deposits are associated with degenerative neural structures and an increased incidence of cells ( microglia, astrocytes). In Alzheimer 's disease, they occur in high densities.

Proof

Usually, the senile plaques by light microscopy after silver plating, staining with Congo red, thioflavin, cresyl violet, PAS reaction, by fluorescence and immunofluorescence microscopy demonstrated.

Occurrence

Senile plaques are found both in human and animal brains (including mammals, birds ). Artificially was created by insertion of human genes, a strain of mice ( transgenic), which forms the precursor protein of Aβ peptides and developed plaques. The occurrence in humans without dementia symptoms may speak for not yet clinically manifest, compensated early stages of a disease process. A small number of senile plaques, however, also occurs in the physiological process of aging. Beyond the age of 60 years ( approximately 10%), the proportion of those affected to about the age of 80 (about 60% ) is approximately linearly. Women are slightly more often affected than men. Most often occur on the plaques in the amygdala and in the cortex Windungstälern.

History

Paul Oscar Blocq and Gheorghe Marinescu 1892 described plaques in the gray matter. Due to the microscopic resemblance to Actinomyces drusen plaques beginning of the 20th century by O. Fischer were called drusige necrosis. The occurrence of plaques associated with dementia has been described by Alois Alzheimer in 1906. Bielschowsky already suspected in 1911 amyloid deposits as significant for their development. Since the beginning of the 20th century relations between Alzheimer's disease, the presence of senile plaques, tangles and angiopathic changes were made. Wisniewski called the deposits 1973 " neuritic plaques ". Also in the 70s of the 20th century saw the hypotheses on immunological and genetic factors in plaque formation ( Katenkamp, Op den Velde and Stam ). Extensive statistical studies from this period JAN Corsellis and M. Franke. Franke showed that a dementia -causing disease process is probably from a plaque density of more than 200/mm ³ frontal cortex. It also supports the hypothesis that hormonal factors for plaque formation have a meaning ( women with tumors have a reduced plaque formation ). Only at the end of the 20th century, the essential components of the plaques were extensively researched (eg, 1985, the Aβ peptides were identified biochemically ), but still have many issues of education and importance, and in particular the issues of possibilities of influencing these processes openly.

Origin and Description

The plaques have different shape and size ( average 50 microns ). According to their variable appearance and composition can further differentiate the senile plaques.

The amyloid senile plaques formed by the deposition of Aβ peptides (39 to 42 mainly amino acids). These polypeptides tend to aggregate and are neurotoxic in a suitable concentration. The aggregate formation in brain tissue appears to be the result of years of interplay between deposition and degradation processes. Why deposition in the brain and not in other organs, despite occurrence of the peptides takes place in the whole organism, is unclear. In the laser scanning microscope, the three-dimensional structure of the plaques with a porous core and with a decreasing thickness towards the periphery of cover will be described. In certain cases, especially in younger patients ( for example, in Trisomy 21 / Down's syndrome ), the formation has a genetic background (for example, erroneous coding of the amyloid precursor protein APP by point mutation on chromosome 21, the erroneous coding secretases presenilin 1 and 2 on chromosome 14 and chromosome 1). As a genetic risk factor, the epsilon 4 allele of the apolipoprotein E is considered. If there is interference in the degradation of APP, the Aβ peptides are deposited in vessels or in the form of plaques. But further, some as yet unknown factors, probably hormonal, immunological, inflammatory processes, diseases of fat and sugar metabolism play a role in plaque formation.

Importance

The senile plaques are in addition to pathological neurofibrillary tangles, neuropil threads and vacuolar degeneration, hirnatrophischen changes with hydrocephalus e vacuo important criteria of neuro- pathological- histological postmortem detection of Alzheimer 's disease. The emergence and the distribution pattern of neurofibrillary tangles and neuropil follows a certain law ( Braak and Braak ) and allows staging. Together with the occurrence of many senile plaques is to make a diagnosis of Alzheimer 's disease with high probability. In theory, so that the foundations of a hirnbioptische investigation would be set, but the intervention is not justified in still unsatisfactory therapeutic options and diagnostic alternatives such as positron emission tomography.