Brain pathology

Brengel-Pesce K, Innocenti-Francillard P, Morand P, Chanzy B, Seigneurin JM (1997) Transient infection of astrocytes with HIV-1 primary isolates derived from patients with and without AIDS dementia complex. J Neurovirol 3 449-454 Budka H, Costanzi G, Cristina S, Lechi A, Parravicini C, Trabattoni R, Vago L (1987) Brain pathology induced by infection with the human immunodeficiency virus (HIV). A histological, immunocytochemical, and electron microscopical study of 100 autopsy cases. Acta Neuropathol (Berl) 75 185-198... 

Braak H., Tredici K., Rub U. et al. (2003). Staging of brain pathology related to sporadic Parkinson s disease. Neurobiol. Aging 24, 197-211. 

Matsuda, J., Suzuki, O., Oshima, A. et al. Chemical chaperone therapy for brain pathology in GM1-gangliosidosis. Proc. Natl Acad. Sci. U.S.A. 100 15912-15917,2003. 

Gy, whole body, single exposure No brain pathology 44... 

Although ubiquitin was used as a marker for brain pathology, no physiological or pathological role for ubiquitin in the nervous system was found until about a decade ago. The first discovery of ubiquitin—proteasome-mediated degradation of a physiologically relevant substrate in the nervous system was that of R subunits of PKA. Since then several substrates of the ubiquitin—proteasome pathway in the nervous system have been identified (Table 6). 

FIGURE 12—14. Postmortem brain pathology defines what Alzheimer s disease is. Shown here are abnormal degenerative structures called neuritic plaques with amyloid cores. 

Fig. 6.7 Filipin staining for free cholesterol in field CA3 of the hippocampus. A section from a normal rat, showing light staining for free cholesterol in pyramidal neurons (arrows). B section from a rat that had been injected with kainate 1 day earlier, showing intense filipin staining in affected hippocampal neurons (arrows). Scale = 250 // m. Reproduced with kind permission from Ong et al., 2003, Brain Pathology 13 250-262. Blackwell Publishing...

X-ALD is a disorder of peroxisomal P-oxidation of VLCFA and is estimated to occur in approximately 1 20,000 males. The first description of an affected patient was in 1910. This patient was a previously healthy boy who developed visual disturbances at the age of 6 years, followed by deterioration of his schoolwork, and then spastic gait. His older brother had died of a similar illness in childhood. The brain pathology in this child revealed diffuse loss of myelin in the cerebral hemispheres. Involvement of the adrenal gland was subsequently reported in later-identified patients,... 

Patients with acute and chronic Al encephalopathy can demonstrate unilateral or bilateral myoclonic jerks of the extremities for several months in the chronic form and days to weeks in the acute form, followed by convulsions and coma even when the exposure is terminated, ft seems as if brain pathology reaches a point of no return which results in frequent epileptic insults and inevitably leads to coma and death, either due to superimposed infections like aspiration pneumonia, or pulmonary edema due to cardiac toxicity. Recovery is exceptional in severe cases. In the past, reports showed that the early stages of chronic Al encephalopathy progressed to death, mainly because the most important source of Al, namely the dialysis fluid contamination, was not recognized as such and the exposure continued for months to years [10-17, 19-42]. 

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