Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling

Alzheimer disease (AD) is a heterogeneous neurodegenerative disorder characterized by (1) progressive loss of synapses and neurons, (2) intracellular neurofibrillary tangles, composed of hyperphosphorylated Tau protein, and (3) amyloid plaques. Genetically, AD is linked to mutations in few proteins...

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Main Authors: Nizzari, Mario, Thellung, Stefano, Corsaro, Alessandro, Villa, Valentina, Pagano, Aldo, Porcile, Carola, Russo, Claudio, Florio, Tullio
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306972/
id pubmed-3306972
recordtype oai_dc
spelling pubmed-33069722012-04-11 Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling Nizzari, Mario Thellung, Stefano Corsaro, Alessandro Villa, Valentina Pagano, Aldo Porcile, Carola Russo, Claudio Florio, Tullio Review Article Alzheimer disease (AD) is a heterogeneous neurodegenerative disorder characterized by (1) progressive loss of synapses and neurons, (2) intracellular neurofibrillary tangles, composed of hyperphosphorylated Tau protein, and (3) amyloid plaques. Genetically, AD is linked to mutations in few proteins amyloid precursor protein (APP) and presenilin 1 and 2 (PS1 and PS2). The molecular mechanisms underlying neurodegeneration in AD as well as the physiological function of APP are not yet known. A recent theory has proposed that APP and PS1 modulate intracellular signals to induce cell-cycle abnormalities responsible for neuronal death and possibly amyloid deposition. This hypothesis is supported by the presence of a complex network of proteins, clearly involved in the regulation of signal transduction mechanisms that interact with both APP and PS1. In this review we discuss the significance of novel finding related to cell-signaling events modulated by APP and PS1 in the development of neurodegeneration. Hindawi Publishing Corporation 2012 2012-02-08 /pmc/articles/PMC3306972/ /pubmed/22496686 http://dx.doi.org/10.1155/2012/187297 Text en Copyright © 2012 Mario Nizzari et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Nizzari, Mario
Thellung, Stefano
Corsaro, Alessandro
Villa, Valentina
Pagano, Aldo
Porcile, Carola
Russo, Claudio
Florio, Tullio
spellingShingle Nizzari, Mario
Thellung, Stefano
Corsaro, Alessandro
Villa, Valentina
Pagano, Aldo
Porcile, Carola
Russo, Claudio
Florio, Tullio
Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
author_facet Nizzari, Mario
Thellung, Stefano
Corsaro, Alessandro
Villa, Valentina
Pagano, Aldo
Porcile, Carola
Russo, Claudio
Florio, Tullio
author_sort Nizzari, Mario
title Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
title_short Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
title_full Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
title_fullStr Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
title_full_unstemmed Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling
title_sort neurodegeneration in alzheimer disease: role of amyloid precursor protein and presenilin 1 intracellular signaling
description Alzheimer disease (AD) is a heterogeneous neurodegenerative disorder characterized by (1) progressive loss of synapses and neurons, (2) intracellular neurofibrillary tangles, composed of hyperphosphorylated Tau protein, and (3) amyloid plaques. Genetically, AD is linked to mutations in few proteins amyloid precursor protein (APP) and presenilin 1 and 2 (PS1 and PS2). The molecular mechanisms underlying neurodegeneration in AD as well as the physiological function of APP are not yet known. A recent theory has proposed that APP and PS1 modulate intracellular signals to induce cell-cycle abnormalities responsible for neuronal death and possibly amyloid deposition. This hypothesis is supported by the presence of a complex network of proteins, clearly involved in the regulation of signal transduction mechanisms that interact with both APP and PS1. In this review we discuss the significance of novel finding related to cell-signaling events modulated by APP and PS1 in the development of neurodegeneration.
publisher Hindawi Publishing Corporation
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306972/
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