Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Neuronal localization of the TNF alpha converting enzyme (TACE) in brain tissue and its correlation to amyloid plaques
Autore:
Skovronsky, DM; Fath, S; Lee, VMY; Milla, ME;
Indirizzi:
Univ Penn, Sch Med, Dept Pathol & Lab Med, Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 t Dis Res, Philadelphia, PA 19104 USA Univ Penn, Sch Med, Dept Biochem & Biophys, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 & Biophys, Philadelphia, PA 19104 USA Univ Penn, Sch Med, Johnson Res Fdn, Philadelphia, PA 19104 USA Univ PennPhiladelphia PA USA 19104 n Res Fdn, Philadelphia, PA 19104 USA
Titolo Testata:
JOURNAL OF NEUROBIOLOGY
fascicolo: 1, volume: 49, anno: 2001,
pagine: 40 - 46
SICI:
0022-3034(200110)49:1<40:NLOTTA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; FAMILIAL ALZHEIMERS-DISEASE; HUMAN CELL-LINE; PRECURSOR PROTEIN; SECRETASE CLEAVAGE; BETA-SECRETASE; NTERA-2 CELLS; IN-VIVO; PRESENILIN-1; DISINTEGRIN;
Keywords:
TACE; amyloid precursor protein; alpha-secretase; beta-secretase; Alzheimer's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Milla, ME Univ Penn, Sch Med, Dept Pathol & Lab Med, Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Philadelphia, PA 19104 USA
Citazione:
D.M. Skovronsky et al., "Neuronal localization of the TNF alpha converting enzyme (TACE) in brain tissue and its correlation to amyloid plaques", J NEUROBIOL, 49(1), 2001, pp. 40-46

Abstract

The tumor necrosis factor (TNF)-alpha converting enzyme (TACE) can cleave the cell-surface ectodomain of the amyloid-beta precursor protein (APP), thus decreasing the generation of amyloid-beta (A beta) by cultured non-neuronal cells. While the amyloidogenic processing of APP in neurons is linked to the pathogenesis of Alzheimer's disease (AD), the expression of TACE in neurons has not yet been examined. Thus, we assessed TACE expression in a series of neuronal and non-neuronal cell types by Western blots. We found that TACE was present in neurons and was only faintly detectable in lysates ofastrocytes, oligodendrocytes, and microglial cells. Immunohistochemical analysis was used to determine the cellular localization of TACE in the humanbrain, and its expression was detected in distinct neuronal populations, including pyramidal neurons of the cerebral cortex and granular cell layer neurons in the hippocampus. Very low levels of TACE were seen in the cerebellum, with Purkinje cells at the granular-molecular boundary staining faintly. Because TACE was localized predominantly in areas of the brain that are affected by amyloid plaques in AD, we examined its expression in a series of AD brains. We found that AD and control brains showed similar levels of TACE staining, as well as similar patterns of TACE expression. By double labeling for A beta plaques and TACE, we found that TACE-positive neurons often colocalized with amyloid plaques In AD brains. These observations supporta neuronal role for TACE and suggest a mechanism for its involvement in ADpathogenesis as an antagonist of A beta formation. (C) 2001 John Wiley & Sons, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 01:44:51