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  • 1
    ISSN: 1432-0533
    Keywords: Thromboangiitis obliterans ; Dementia ; Cortical synaptophysin expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The generalized form of von Winiwarter-Buerger's disease (WBD) occasionally involves the brain. However, pure cerebral forms of the disease were also described by Spatz and Lindenberg (“Spatz-Lindenberg's disease”, SLD). Both, the type I, which involves the large basal arteries, and the type II, which results in a sickle-shaped granular atrophy of the cerebral cortex, are often accompanied by (“vascular”) dementia, which Lindenberg and Spatz mainly attributed to the bilateral involvement of the second frontal gyrus by granular atrophy. Recently, synaptic deprivation of the cortical gray matter has been shown to occur in the dementia of Alzheimer type (DAT) and other neurodegenerative disorders. In DAT, the synaptic loss highly correlated with the degree of the mental impairment. We wanted to examine whether similar changes also occurred in dementia of vascular origin, for which SLD, although infrequent, is a typical example. In fact, we found that in three cases of typical SLD type II the synaptophysin immunoreactivity of the cortical neuropil in areas without overt infarcts or scar formation was as much reduced as in Alzheimer's disease. Although it must be taken into account that in the present cases the synapse loss might, at least in part, be due to secondary (Wallerian) degeneration as a result of the neuronal loss in the “watershed” regions of the arterial blood supply, it cannot be excluded that a decline of cortical synaptic contacts in areas without necroses or scars may occur as a primary event, contributing to the pathogenesis of the dementia. Final conclusions can only be expected from investigations into further cases of cerebro-vascular disorders with and without dementia.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2307
    Keywords: Alzheimer's disease ; Complement ; Classical pathway
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In Alzheimer's disease (AD) patients, the complement components Clq, C4 and C3 can be detected in different types of β/A4 plaques, one of the hallmarks of AD. Contradictory findings on the presence of late complement components in AD brains have been reported. Nevertheless, it was suggested in recent studies that in AD brain complement activation results in complement membrane attack complex (MAC) formation and that complement activation may act as an intermediate between β/A4 deposits and the neurotoxicity observed in AD. In the present study the presence of a number of complement components and regulatory proteins in AD temporal cortex and, for comparison, in glomerulone-phritis (GN) was analysed. In GN kidneys, besides Clq, Clr, Cls and C3, the late components and the C5b-9 complex are also associated with capillary basement membrane and mesangial immune complex deposits. In AD temporal cortex Clq, C4 and C3 are co-localized with β/A4 deposits. However, in contrast to the GN kidney, the late complement components C5, C7 and C9, as well as the C5b-9 membrane attack complex cannot be detected in β/A4 positive plaques. The absence of the cytolytic C5b-9 complex in AD brain suggests that in AD, the complement MAC does not function as the proposed inflammatory mediator between β/A4 deposits and the neurofibrillary changes.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Alzheimer's disease ; Altered neurites ; Neuropil threads ; Growth-promoting factors ; Tau-related cytoskeletal pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the present immunohistochemical study, we investigated the characteristics of altered neurites in the frontal cortex of 10 Alzheimer's disease (AD) brains and 15 age-matched non-demented control brains. In both AD and control cases, the altered neurites in coronas of the classical plaques (CP) were frequently immunostained by antibodies to growth-promoting factors, N and C termini of amyloid precursor protein (APP), GAP43, collagen IV, laminin and th e integrin receptor VLA6. The altered neurites in CP coronas in AD but not in controls were also immunostained by antibodies against normally and abnormally phosphorylated tau. Immunolabeling for microtubule-associated protein 2 was not found in CP from either group. Extensive neuropil threads (NT) and many neurofibrillary tangles (NFT), immunostained with tau and Alz50 antibodies, were present in AD neocortex but not seen in control cases. NT and NFT could not be stained by antibodies to the N termini of A PP, GAP43, collagen IV, laminin and VLA6. Our findings indicate that in AD cases altered neurites in CP are undergoing both an aberrant sprouting process and a degenerating process. These altered neurites are probably of axon origin. NT and NFT may represent destructive changes. The presence of amyloid plaques, but absence of tau-related cytoskeletal pathology, in non-demented cases suggests that β/A4 peptide is necessary but not sufficient to induce neurofibrillary pathology.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2307
    Keywords: Adhesion molecules ; Integrins ; Laminin ; Amyloid plaques ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Integrins belonging to different subfamilies can be identified immunohistochemically in cerebral amyloid plaques. Monoclonal antibodies against the VLA family β1-integrins show staining of the corona of classical amyloid plaques for β1, α3 and α6. Immunostaining reveal also the presence of collagen and laminin in the corona. Activated microglial cells in classical plaques strongly express receptors belonging to the LeuCAM family (β2 integrins). The ligands ICAM and activated complement C3 are found in both amorphous and classical plaques. Vitronectin receptor (αv) is found in glial cells in classical plaques but its ligand vitronectin is seen in both amorphous and classical plaques. The data presented here demonstrate the presence of different cellular and substrate adhesive molecules (intregrins) and their ligands in classical plaques. The findings suggest that amyloid plaques show signs of regeneration and tissue remodelling.
    Type of Medium: Electronic Resource
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