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Titolo:
Hereditary cerebral amyloid angiopathy
Autore:
Gray, F; Chretien, F; Keohane, C;
Indirizzi:
Hop Ray Poincare, Neuropathol Lab, Paris, France Hop Ray Poincare Paris France Poincare, Neuropathol Lab, Paris, France Cork Univ Hosp, Dept Pathol, Cork, Ireland Cork Univ Hosp Cork IrelandCork Univ Hosp, Dept Pathol, Cork, Ireland
Titolo Testata:
REVUE NEUROLOGIQUE
fascicolo: 10, volume: 157, anno: 2001,
pagine: 1207 - 1217
SICI:
0035-3787(200110)157:10<1207:HCAA>2.0.ZU;2-7
Fonte:
ISI
Lingua:
FRE
Soggetto:
FAMILIAL OCULOLEPTOMENINGEAL AMYLOIDOSIS; AUTOSOMAL-DOMINANT ARTERIOPATHY; CREUTZFELDT-JAKOB-DISEASE; ONSET ALZHEIMERS-DISEASE; CYSTATIN-C AMYLOIDOSIS; FINNISH TYPE FAF; HCHWA-D; PRION PROTEIN; LEPTOMENINGEAL AMYLOIDOSIS; SPONGIFORM ENCEPHALOPATHY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
95
Recensione:
Indirizzi per estratti:
Indirizzo: Gray, F Hop Ray Poincare, Serv Anat Pathol, 104 Blvd Raymond Poincare, F-92380 Garches, France Hop Ray Poincare 104 Blvd Raymond Poincare Garches France F-92380
Citazione:
F. Gray et al., "Hereditary cerebral amyloid angiopathy", REV NEUROL, 157(10), 2001, pp. 1207-1217

Abstract

Cerebral amyloid angiopathies are defined by the presence of amyloid substance in the walls of cerebral vessels. All amyloid substances have a particular physico-chemical structure, which imparts certain specific staining properties, but the biochemical composition of different amyloid types varies. Different forms of cerebral amyloid angiopathy have been identified, based on the biochemical nature of the protein deposited (e.g. beta-amyloid, cystatin C, transthyretin, gelsolin, amyloid protein Brl, prion protein). Some cerebral amyloid angiopathies are familial; these prompted genetic studies which in turn led to a better understanding of the genes coding for different amyloid proteins. As a group, cerebral amyloid angiopathies have certain neuropathological lesions in common. Infiltration by amyloid substance results in weakening ofthe small vessel walls and secondary complications responsible for changessuch as microinfarcts and miliary haemorrhages in the cerebral cortex, lobar haemorrhages and/or leucoencephalopathy. These changes form the basis ofthe neurological complications: meningeal and cerebral haemorrhages, transient ischaemic episodes, vascular dementia. However each type of hereditarycerebral amyloid angiopathy has individual clinical and histopathological features reflecting the severity of arterial involvement, the extent of amyloid deposition within or outside the central nervous system, and the association with other neurodegenarative changes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 20:55:41