By Vladimir N. Uversky (Editor), Anthony Fink (Editor)
The second one quantity maintains to fill the distance in protein overview and protocal literature whereas summarizing fresh achievements within the knowing of the relationships among protein misfoldings, aggregation, and improvement of protein deposition problems. the point of interest of half B is the molecular foundation of differential issues.
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Extra info for Protein Misfolding, Aggregation and Conformational Diseases (Protein Reviews)
Example text
Punctate and stelate deposits are less than 5 m in size and are frequently found in the vicinity of focal or diffuse plaques (Duyckaerts and Dickson, 2003). , 2001). , 2001). They consist of A42 and stain with hematoxylin-eosin but not with Congo red. As their name implies, they look like cotton balls. They are frequently seen in association with moderate to advanced cerebral amyloidosis (Duyckaerts and Dickson, 2003). In addition to plaques, A deposits are found in the small arteries, veins, and capillaries of cerebral and cerebellar cortices and the leptomeninges.
The connectivity model for AD proposes that the selective neuronal vulnerability is determined by afferent and efferent connections with other cortical areas. The connectionist’s argument is based on the fact that the long corticocortical projection neurons are subjected to alzheimerization, whereas the short corticocortical projection neurons remain unaffected. They also argue that the AD stages represent a stepwise retrograde hierarchical “travel” of the pathology along intrahemispheric corticocortical tracts from the anatomically simpler allo- and periallocortical areas to the very complex neocortex.
2004). A disturbance of late myelination as a trigger for Alzheimer’s disease. Neurobiol Aging 25: 41–43. , McKeel, D. , Miller, J. , Rubin, E. , Morris, J. , Goate, A. , Price, J. , Mirra, S. S. and Saunders, A. M. (1998). Clinicopathologic studies in cognitively healthy aging and Alzheimer’s disease: relation of histologic markers to dementia severity, age, sex, and apolipoprotein E genotype. Arch Neurol 55: 326–335. Bertoli Avella, A. , Llibre Rodriguez, J. , Severijnen, E. , van Duijn, C. , Heredero Baute, L.