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  • Parkinson’s disease  (2)
  • Reticular formation  (1)
  • 1
    ISSN: 1432-0533
    Keywords: Key words Parkinson’s disease ; α-Synuclein ; Limbic ¶system ; Motor system ; Reticular formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pathological changes which consistently develop in the lower brain stem of patients suffering from Parkinson’s disease are described against the background of the internal organization and interconnections of the involved nuclei, i.e., the gigantocellular reticular nucleus, bulbar raphe nuclei, and coeruleus-subcoeruleus area. Immunoreactions against the presynaptic protein α-synuclein reveal not only the voluminous forms of Lewy bodies and Lewy neurites but also the otherwise inconspicuous dot- or thread-like types. These lesions develop solely in specific neuronal types. Lipofuscin- or neuromelanin-laden projection cells which at the same time generate a long, unmyelinated or sparsely myelinated axon are particularly susceptible to developing the changes. The bulbar nuclei under consideration receive strong input from supramedullary sources, above all from higher order centers of the limbic system such as the central amygdalar nucleus, periaqueductal gray, and parabrachial nuclei. In turn, they generate descending projections to premotor and motor neurons of the somatomotor system. The disease-related deterioration of both the supramedullary limbic centers and the bulbar brain stem nuclei reduces the limbic influence and markedly impairs the control of premotor and motor neurons. This functional deficit most probably contributes to the overall dysfunction of the motor system typically evolving in the course of Parkinson’s disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Capillary ultrastructure ; Cerebral hypoperfusion ; Parkinson’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cerebral capillaries represent a major interface between the general circulation and the central nervous system and are responsible for sufficient and selective nutrient transport to the brain. Structural damage or dysfunctioning carrier systems of such an active barrier leads to compromised nutrient trafficking. Subsequently, a decreased nutrient availability in the neural tissue may contribute to hampered neuronal metabolism, hence to behavioral and cognitive functional deficiencies. Here we focus on the ultrastrucutral abnormalities of cerebral microvessels in Alzheimer’s disease (AD; n = 5) and Parkinson’s diseasse (PD; n = 10). The capillary microanatomy in samples from the cingulate cortex was investigated by electron microscopy and severe damage to the vessel walls was observed. Characteristic pathological changes including capillary basement membrane thickening and collagen accumulation in the basement membrane were enhanced in both AD and PD. The incidence of capillaries with basement membrane deposits was two times higher in AD and PD than in age-matched controls. Degenerative pericytes in all groups appeared at a similar frequency. The data indicate that basement membrane deposists, as opposed to pericytic degeneration, represent an important pathological feature of AD and PD and suggest that capillary dysfunction may play a causal role in the development of these two major neurodegenerative diseases.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Lewy body ; Parkinson’s disease ; Alzheimer’s disease ; Microglia ; Complement
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inflammatory mechanisms have been demonstrated in Alzheimer’s disease (AD) but their presence in other neurodegenerative disorders is not well documented. Complement factors and activated microglia have been reported in the substantia nigra of Parkinson’s disease (PD). In the present study we investigated the cingulate gyrus of 25 autopsied patients with clinically and neuropathologically well-documented PD, with or without dementia, for the presence of (activated) microglial cells and their relation with Lewy body (LB)-bearing neurons. In addition, we studied the presence of complement factors in LBs. Of the 25 patient, 15 were clinically demented, fulfilling criteria for dementia with LBs (DLB); 7 also fulfilled CERAD morphological criteria for probable or definite Alzheimer type of dementia. Microglia clustering was seen around congophilic plaques with or without tau pathology. Microglial cells were not associated with LB-bearing neurons or noncongophilic plaques. The cortex of DLB patients without AD plaques did not show more microglial cells than the cortex of non-demented controls. The number of microglia was the lowest in young control patients who died immediately after trauma. Complement factor C3d was occasionally seen in diffusely ubiquinated neurons but late complement factors were not detected in these neurons. Double staining for complement and α-synuclein was negative, suggesting the absence of complement in LBs. In contrast, AD plaques in the same sections showed complement factors C3c, C3d, C1q and C5–9. In conclusion, we have found no evidence that inflammatory mechanism are involved in LB formation in cerebral cortex.
    Type of Medium: Electronic Resource
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