Literature DB >> 2559163

Amyloidosis of the nervous system.

G G Glenner1, M A Murphy.   

Abstract

Various types of amyloid fibril deposits occur in the nervous system with unique clinical characteristics and pathogeneses. Genetic mutations cause the familial amyloidotic polyneuropathies and acquired polyneuropathies occurring particularly in patients suffering from hypernephromas and myelomas also result from the production of abnormal proteins. Amyloid fibril deposits in cerebral plaques and vessels consisting of beta-protein are seen in acquired and familial Alzheimer's disease and in Down's syndrome individuals over 40 years of age. This amyloid fibril deposition could result from a mutational, transcriptional or post-translational alteration in these pathologic processes with most evidence supporting the latter. Other diseases including hereditary cerebral hemorrhage of the Dutch type and Batten's disease involve beta-amyloid deposition. The features of the familial and transmissible forms of the spongiform encephalopathies are associated with the prion protein which comprises the amyloid fibril deposits in these conditions. This wide variety of nervous system disorders having amyloid deposits as their primary or subsidiary characteristic make studies of these conditions intriguing models for research workers in clinical, pathologic and molecular biologic fields.

Entities:  

Mesh:

Year:  1989        PMID: 2559163     DOI: 10.1016/0022-510x(89)90214-1

Source DB:  PubMed          Journal:  J Neurol Sci        ISSN: 0022-510X            Impact factor:   3.181


  17 in total

1.  Phagocytosis and deposition of vascular beta-amyloid in rat brains injected with Alzheimer beta-amyloid.

Authors:  S A Frautschy; G M Cole; A Baird
Journal:  Am J Pathol       Date:  1992-06       Impact factor: 4.307

2.  Complement neoantigen and vitronectin are components of plaques in amyloid AL neuropathy.

Authors:  G L Zanusso; G Moretto; B Bonetti; S Monaco; N Rizzuto
Journal:  Ital J Neurol Sci       Date:  1992-09

Review 3.  Current status review: cerebral amyloid.

Authors:  L W Duchen
Journal:  Int J Exp Pathol       Date:  1992-08       Impact factor: 1.925

4.  Alzheimer's disease and the beta amyloid gene.

Authors:  P J Harrison
Journal:  BMJ       Date:  1991-06-22

Review 5.  Aβ oligomer-induced synapse degeneration in Alzheimer's disease.

Authors:  Kyle C Wilcox; Pascale N Lacor; Jason Pitt; William L Klein
Journal:  Cell Mol Neurobiol       Date:  2011-05-03       Impact factor: 5.046

Review 6.  Propargylamine-derived multitarget-directed ligands: fighting Alzheimer's disease with monoamine oxidase inhibitors.

Authors:  Irene Bolea; Alejandro Gella; Mercedes Unzeta
Journal:  J Neural Transm (Vienna)       Date:  2012-12-13       Impact factor: 3.575

Review 7.  Danggui-Shaoyao-San: New Hope for Alzheimer's Disease.

Authors:  Xin Fu; QiuHong Wang; ZhiBin Wang; HaiXue Kuang; Pinghui Jiang
Journal:  Aging Dis       Date:  2015-12-20       Impact factor: 6.745

Review 8.  The role of the tripartite glutamatergic synapse in the pathophysiology of Alzheimer's disease.

Authors:  Carolyn C Rudy; Holly C Hunsberger; Daniel S Weitzner; Miranda N Reed
Journal:  Aging Dis       Date:  2015-03-10       Impact factor: 6.745

9.  Biochemical and anatomical redistribution of tau protein in Alzheimer's disease.

Authors:  E B Mukaetova-Ladinska; C R Harrington; M Roth; C M Wischik
Journal:  Am J Pathol       Date:  1993-08       Impact factor: 4.307

Review 10.  Frequency and genetic background of the position 122 (Val----Ile) variant transthyretin gene in the black population.

Authors:  D R Jacobson; J D Reveille; J N Buxbaum
Journal:  Am J Hum Genet       Date:  1991-07       Impact factor: 11.025

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