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  • Intercellular adhesion molecule-1  (1)
  • Key words Alzheimer's disease  (1)
  • 1
    ISSN: 1432-0533
    Keywords: Key words Alzheimer's disease ; Senile plaques ; Microglia ; Lysosomes ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract One of the major histopathological lesions in brains of patients with dementia of the Alzheimer type (DAT) is the senile plaque. Although previous studies have shown that senile plaques are often accompanied by microglial cells, the role of these cells in DAT pathology is still unclear. In an immunohistochemical and immuno-electron microscopical analysis of DAT and control brain tissues we addressed this issue using two monoclonal antibodies (mAbs KP1 and 25F9) directed against lysosomal antigens in monocytes and macrophages. Whereas KP1 stained lysosomes in both resting and activated microglial cells, 25F9-staining was predominantly found in lysosomes of activated microglial cells in classic senile plaques. The number and size of 25F9-positive lysosomes in activated microglial cells was increased compared to 25F9-staining in unaffected areas in DAT and control sections. We conclude that mAb 25F9 is a unique and useful lysosomal marker, with a higher specificity than other known markers, for activated microglial cells associated with classic, but not with diffuse, senile plaques.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Cerebellum ; Intercellular adhesion molecule-1 ; Cerebrovascular ; Inflammation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inflammatory processes have been implicated in the formation of senile plaques in the cerebral cortex of patients with dementia of the Alzheimer type (DAT), since several inflammation-induced proteins are present within these plaques. The relation between inflammatory components and other amyloid β protein (Aβ)-containing lesions of the DAT brain [cerebrovascular amyloidosis (CA) and cerebellar senile plaques] is unclear. We studied the distribution of the inflammation-inducible protein intercellular adhesion molecule-1 (ICAM-1) in CA and in senile plaques of the cerebellum, using an immunohistochemical approach. We observed striking differences in ICAM-1 reactivity between the different types of Aβ-containing lesions. ICAM-1 was only expressed in classic senile plaques in the granular and Purkinje cell layer of the cerebellum, and not in diffuse senile plaques of the molecular layer. Also, ICAM-1 was not associated with CA; only when the vascular amyloid extended into the neuropil (dyshoric angiopathy) was perivascular ICAM-1 reactivity observed. This is in contrast to the putative primary involvement of inflammation in the formation of cerebrocortical classic and diffuse senile plaques. Our findings indicate that ICAM-1 expression, which may be an indicator of an inflammatory reaction, is induced in the neuropil depending on the specific site of Aβ production.
    Type of Medium: Electronic Resource
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