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A morphological analysis of senile plaques in the brains of nondemented persons of different ages using silver, immunocytochemical and lectin histochemical staining techniques
Author(s) -
MANN D. M. A.,
BROWN A. M. T.,
PRINJA D.,
JONES D.,
DAVIES C. A.
Publication year - 1990
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1990.tb00928.x
Subject(s) - grocott's methenamine silver stain , staining , senile plaques , pathology , silver stain , hippocampus , cerebral cortex , cortex (anatomy) , pathological , amyloid (mycology) , immunohistochemistry , alzheimer's disease , biology , medicine , neuroscience , disease
The prevalence and severity of senile plaque (SP) formation was investigated in the cerebral cortex, hippocampus and amygdala of 60 non‐demented individuals of age range 6–84 years, using immunocytochemical (anti‐A4 amyloid, anti‐PHF protein), lectin histochemical (Con A binding) and silver (Methenamine (MS) and Palmgren), staining methods. By at least one of these methods, 18 patients showed the presence of SP within one or more of these brain regions; 15 of these patients were over 60 years of age. Comparisons between each staining method showed that, in the hippocampus and amygdala all five methods detected the presence and number of SP equally well, whereas, in the cerebral cortex, MS and anti‐A4 staining demonstrated more SP in a greater number of patients than did either Con A or Palmgren silver and anti‐PHF staining. The additional SP detected by these former two staining methods contained diffuse deposits of amyloid (A4) protein, and sometimes also large clumps of Con A positive material, but no neurites as detected by Palmgren or anti‐PHF staining. Such SP closely resemble those seen in the cerebral cortex of young patients with Down's syndrome, and which are thought to be an early form of SP. The relationship between the pathological changes in these non‐demented patients and a possible diagnosis of early Alzheimer's disease is discussed.