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Titolo:
Intracellular APP processing and A beta production in Alzheimer disease
Autore:
Wilson, CA; Doms, RW; Lee, VMY;
Indirizzi:
Univ Penn, Sch Med, Dept Pathol & Lab Med, Med Ctr,Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 t Dis Res, Philadelphia, PA 19104 USA
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 8, volume: 58, anno: 1999,
pagine: 787 - 794
SICI:
0022-3069(199908)58:8<787:IAPAAB>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; SENILE PLAQUES; SECRETASE CLEAVAGE; TRANSGENIC MICE; NEUROFIBRILLARY TANGLES; HUMAN NEURONS; NT2N CELLS; MECHANISMS; PEPTIDE; COMPARTMENT;
Keywords:
intracellular A beta; insoluble A beta 42; endoplasmic reticulum; senile plaques;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Lee, VMY Univ Penn, Sch Med, Dept Pathol & Lab Med, Med Ctr,Ctr Neurodegenerat Dis Res, Maloney 3,HUP, Philadelphia, PA 19104 USA Univ Penn Maloney 3,HUP Philadelphia PA USA 19104 a, PA 19104 USA
Citazione:
C.A. Wilson et al., "Intracellular APP processing and A beta production in Alzheimer disease", J NE EXP NE, 58(8), 1999, pp. 787-794

Abstract

Senile plaques composed of A beta peptides are a histopathological hallmark of Alzheimer disease (AD). A role for A beta in the etiology of AD has been argued from analysis of mutations associated with a subset of early-onset familial AD (FAD). Expression of autosomal dominant mutations in the genes for the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) in affected patients, cultured cells, or transgenic mice leads to increased production of total A beta or increased production of A beta ending at residue 42(A beta 42). Since A beta 42 is the more amyloidogenic and toxic species in vitro and is the major component of amyloid senile plaques in vivo, overproduction of this peptide may play a crucial role in the pathogenesis of AD. Thus, an understanding of the production of A beta within the cell in normal and pathological conditions is critical to understanding early events in AD. Studies in cell culture have established that processing of APP to form A beta can occur at multiple locations within the cell and leads to the production of 2 pools of A beta: a secreted pool composed predominantly of A beta 40 and a nonsecreted, intracellular pool composed preferentially of more amyloidogenic A beta 42. The purpose of this review is to provide a summary of our current understanding of APP processing in the generation of the secreted and intracellular pools of A beta and to propose a model linking the intracellular pool to the formation of extracellularplaques and neuronal pathology in AD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 02:09:11