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  • 1
    Electronic Resource
    Electronic Resource
    Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer’s disease: histotopographical correlation with amyloid plaques and hyperphosphorylated-tau protein (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well-known features accompanying the cognitive dysfunction seen in Alzheimer’s disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (α4, α7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch-clamp recordings of 14 dissociated neurons of control cortices showed responses suggesting the existence of α4- and α7-containing functional nAChRs in the human cortex. In cortices of Alzheimer patients and controls, the pattern of distribution and the number of α4 and α7 mRNA-expressing neurons were similar, whereas at the protein level a decrease in the density of α4- and α7-expressing neurons of ≈ 30% was observed in Alzheimer patients. The histotopographical correlation of nAChR expression with accompanying pathological changes, e.g. accumulation of hyperphosphorylated-tau (HP-tau) protein and β-amyloid showed that neurons in the vicinity of β-amyloid plaques bore both nAChR transcripts. Neurons heavily labelled for HP-tau, however, expressed little or no α4 and α7 mRNA. These results point to an impaired synthesis of nAChRs on the protein level as a possible cause of the cholinoceptive deficit in AD. Further investigations need to elucidate whether interactions of HP-tau with nAChR mRNA, or alterations in the quality of α4 and α7 transcripts give rise to decreased protein expression at the level of individual neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00676.x
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  • 2
    Electronic Resource
    Electronic Resource
    Amygdala pathology in Parkinson's disease (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 493-500 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amygdala ; Lewy body ; Parkinson's ; disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The amygdala undergoes severe pathological changes during the course of Parkinson's disease (PD). Lewy bodies and Lewy neurites are distributed in a specific manner throughout the nuclear complex. The lesional pattern displays only minor interindividual variation. The most prominent changes occur in the accessory cortical and central nuclei. The cortical, accessory basal and granular nuclei show less severe alterations, while the basal and lateral nuclei, as well as the intercalated cell masses, generally remain uninvolved. The amygdala receives a broad range of afferents, allowing integration of exteroceptive information with interoceptive data. It generates major projections to the isocortex (the prefrontal cortex in particular), limbic system (hippocampus and entorhinal region) and centers regulating endocrine and autonomic functions. The specific lesional pattern seen in PD destroys part of the nuclear gray matter and its connections and, thus, may likely contribute to the development of behavioral changes and autonomic dysfunctions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296485
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  • 3
    Electronic Resource
    Electronic Resource
    Parkinson’s disease: affection of brain stem nuclei controlling premotor and motor neurons of the somatomotor system (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 489-495 
    Details
    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
    URL: http://dx.doi.org/10.1007/s004010051150
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  • 4
    Electronic Resource
    Electronic Resource
    Activated microglial cells and complement factors are unrelated to cortical Lewy bodies (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 701-708 
    Details
    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
    URL: http://dx.doi.org/10.1007/s004010000225
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Pathological features of cerebral cortical capillaries are doubled in Alzheimer’s disease and Parkinson’s disease (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 395-402 
    Details
    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
    URL: http://dx.doi.org/10.1007/s004010000195
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    Paper (German National Licenses)
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