By Arthur K. Asbury, Guy M. McKhann, W. Ian McDonald, Peter J. Goadsby, Justin C. McArthur
The 3rd version of a neurology vintage, this two-volume textual content is the main finished neurology reference to be had. Written by way of major overseas specialists within the box, it encompasses the elemental neuroscience and medical positive factors of the whole diversity of neurological issues. illness mechanisms are reviewed comprehensively, with specific relevance to the foundations of remedy. every one part, less than the path of 1 of the celebrated editors, is a text-within-a-text, supplying the main trustworthy account of its subject at present on hand.
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Extra info for Diseases of the Nervous System: Clinical Neuroscience and Therapeutic Principles
Arthur K. Asbury Guy M. McKhann W. Ian McDonald Peter J. Goadsby Justin C. McArthur Part I Introduction and general principles 1 Pathophysiology of nervous system diseases Justin C. McArthur1, Guy M. McKhann2, W. Ian McDonald3, Peter J. Goadsby4 and Arthur K. Asbury5 2 1 Departments of Neurology and Epidemiology, Johns Hopkins University Baltimore, MD, USA The Zanvyl Krieger Mind and Brain Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA 3 Institute of Neurology, University College London, Royal College of Physicians, London, UK 4 Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, UK 5 University of Pennsylvania School of Medicine, Philadelphia, PA, USA Since the last edition of this textbook, the ﬁeld of Neurology and the Neurosciences has witnessed remarkable advances in the technologies available for the study of the brain and our concepts about the nervous system and its diseases.
2. Proposed mechanism of huntingtin-induced death of neuronal cells. The mutant huntingtin protein produced by an increase in the number of CAG repeats in the DH gene is cleaved to fragments that retain the increased number of glutamine residues. These fragments are conjugated with ubiquitin and carried to the proteasome complex. Subsequent cleavage is incomplete, and components of both huntingtin and the proteasome are translocated to the nucleus, where aggregates form, resulting in intranuclear inclusions.
O. (1999). Emerging insights into the genesis of epilepsy. Nature, 399, A15–A22. , Tassorelli, C. M. (2000). Migraine as a complex disease: heterogeneity, comorbidity and genotype–phenotype interactions. Funct. , 15, 87–93. J. (2001). Neurobiology. Total recall – the memory of addiction. Science, 292, 2266–7. , Benussi, L. et al. (2001). Analysis of alpha2-macroglobulin-2 allele as a risk factor in alzheimer’s disease. Dement. Geriatr. Cogn. , 12, 305–8. F. et al. (2001). Interference by huntingtin and atrophin-1 with cbp-mediated transcription leading to cellular toxicity.
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