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  • 1
    ISSN: 1432-0533
    Keywords: Key words Presenilin ; Alzheimer’s disease ; Immunohistochemistry ; Golgi apparatus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The immunolocalization of presenilin in human brain was studied using two antibodies raised against different portions of presenilin 1 (S182) protein. A granular staining was found in the cytoplasm of neurons in cortical layers III and V. One of the antibodies, also reactive to presenilin 2 (E5-1) protein, additionally stained dendrites and axons. This was seen in normal brains as well as in brains affected by Alzheimer’s disease. Less prominent immunolabeling was noted in some senile plaques. No relationship to neurofibrillary tangles was found in double-labeling experiments combined with anti-paired helical filament-tau antibody (AT8). The widespread expression of presenilin in normal brain suggests a physiological role of the protein.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E ; APOE genotype ; Alzheimer’s disease ; Senile plaque
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to analyze the relationship between apolipoprotein E (ApoE) and amyloid β-protein (Aβ) deposits in 29 brains from a series of elderly women, whose intellectual status had been prospectively assessed by the Blessed test score (BTS). In three cases the APOE genotype was ɛ3/4, in one ɛ2/2, in 25 ɛ3/3. ApoE-like immunoreactive lesions resembling a classic senile plaque (ApoE-SP) or a diffuse deposit (ApoE-DD) were quantitatively assessed in the first temporal gyrus (Brodmann’s area 22). The density of ApoE-positive deposits (ApoE-SP+ApoE-DD) was correlated with BTS (negative correlation R 2 = 0.36, P = 0.0006). The correlation of the density of ApoE-DD with BTS (R 2 = 0.26, P = 0.0051) was weaker than that of ApoE-SP (R 2 = 0.50, P 〈 0.0001). The density of ApoE deposits was correlated with that of Aβ-immunoreactive lesions (positive correlation R 2 = 0.57, P 〈 0.0001). ApoE immunohistochemistry labeled fewer deposits than Aβ immunohistochemistry but showed as many senile plaques (ApoE-SP) as tau immunohistochemistry and the Gallyas and Bodian techniques. Two of the three cases with the ɛ3/4 allele had Alzheimer’s disease (AD) with numerous ApoE-immunoreactive senile plaques. In contrast, the brain of the third ɛ3/4 case, whose intellectual status was normal, contained numerous Aβ deposits but lacked ApoE-like immunoreactivity. The presence of ApoE may, thus, not be a prerequisite for Aβ deposition, even in cases with the ɛ3/4 allele. The density of ApoE-SP peaked in layer III, whereas that of ApoE-DD was maximal in deeper cortical layers. This contrast in the laminar distribution indicates that only some ApoE-DD may evolve into ApoE-SP. ApoE deposition was linked to the intellectual decline and was constant in the most severely demented patients, in whom numerous ApoE-positive (and Aβ-positive) neuritic plaques were surrounded by dystrophic neurites. ApoE may accumulate in neuritic senile plaques during the progression of AD.
    Type of Medium: Electronic Resource
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