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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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/ |
_version_ |
1611515199702958080 |