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Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development

The hyperphosphorylation of tau protein and the overexpression of mTOR are considered to be the driving force behind Aβ plaques and Neurofibrillay Tangles (NFT's), hallmarks of Alzheimer's disease (AD). It is now evident that miscellaneous diseases such as Diabetes, Autoimmune diseases, Ca...

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Autores principales: Mueed, Zeba, Tandon, Pallavi, Maurya, Sanjeev Kumar, Deval, Ravi, Kamal, Mohammad A., Poddar, Nitesh Kumar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335350/
https://www.ncbi.nlm.nih.gov/pubmed/30686983
http://dx.doi.org/10.3389/fnins.2018.01017
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author Mueed, Zeba
Tandon, Pallavi
Maurya, Sanjeev Kumar
Deval, Ravi
Kamal, Mohammad A.
Poddar, Nitesh Kumar
author_facet Mueed, Zeba
Tandon, Pallavi
Maurya, Sanjeev Kumar
Deval, Ravi
Kamal, Mohammad A.
Poddar, Nitesh Kumar
author_sort Mueed, Zeba
collection PubMed
description The hyperphosphorylation of tau protein and the overexpression of mTOR are considered to be the driving force behind Aβ plaques and Neurofibrillay Tangles (NFT's), hallmarks of Alzheimer's disease (AD). It is now evident that miscellaneous diseases such as Diabetes, Autoimmune diseases, Cancer, etc. are correlated with AD. Therefore, we reviewed the literature on the causes of AD and investigated the association of tau and mTOR with other diseases. We have discussed the role of insulin deficiency in diabetes, activated microglial cells, and dysfunction of blood-brain barrier (BBB) in Autoimmune diseases, Presenilin 1 in skin cancer, increased reactive species in mitochondrial dysfunction and deregulated Cyclins/CDKs in promoting AD pathogenesis. We have also discussed the possible therapeutics for AD such as GSK3 inactivation therapy, Rechaperoning therapy, Immunotherapy, Hormonal therapy, Metal chelators, Cell cycle therapy, γ-secretase modulators, and Cholinesterase and BACE 1-inhibitors which are thought to serve a major role in combating pathological changes coupled with AD. Recent research about the relationship between mTOR and aging and hepatic Aβ degradation offers possible targets to effectively target AD. Future prospects of AD aims at developing novel drugs and modulators that can potentially improve cell to cell signaling, prevent Aβ plaques formation, promote better release of neurotransmitters and prevent hyperphosphorylation of tau.
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spelling pubmed-63353502019-01-25 Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development Mueed, Zeba Tandon, Pallavi Maurya, Sanjeev Kumar Deval, Ravi Kamal, Mohammad A. Poddar, Nitesh Kumar Front Neurosci Neuroscience The hyperphosphorylation of tau protein and the overexpression of mTOR are considered to be the driving force behind Aβ plaques and Neurofibrillay Tangles (NFT's), hallmarks of Alzheimer's disease (AD). It is now evident that miscellaneous diseases such as Diabetes, Autoimmune diseases, Cancer, etc. are correlated with AD. Therefore, we reviewed the literature on the causes of AD and investigated the association of tau and mTOR with other diseases. We have discussed the role of insulin deficiency in diabetes, activated microglial cells, and dysfunction of blood-brain barrier (BBB) in Autoimmune diseases, Presenilin 1 in skin cancer, increased reactive species in mitochondrial dysfunction and deregulated Cyclins/CDKs in promoting AD pathogenesis. We have also discussed the possible therapeutics for AD such as GSK3 inactivation therapy, Rechaperoning therapy, Immunotherapy, Hormonal therapy, Metal chelators, Cell cycle therapy, γ-secretase modulators, and Cholinesterase and BACE 1-inhibitors which are thought to serve a major role in combating pathological changes coupled with AD. Recent research about the relationship between mTOR and aging and hepatic Aβ degradation offers possible targets to effectively target AD. Future prospects of AD aims at developing novel drugs and modulators that can potentially improve cell to cell signaling, prevent Aβ plaques formation, promote better release of neurotransmitters and prevent hyperphosphorylation of tau. Frontiers Media S.A. 2019-01-10 /pmc/articles/PMC6335350/ /pubmed/30686983 http://dx.doi.org/10.3389/fnins.2018.01017 Text en Copyright © 2019 Mueed, Tandon, Maurya, Deval, Kamal and Poddar. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Mueed, Zeba
Tandon, Pallavi
Maurya, Sanjeev Kumar
Deval, Ravi
Kamal, Mohammad A.
Poddar, Nitesh Kumar
Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title_full Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title_fullStr Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title_full_unstemmed Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title_short Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
title_sort tau and mtor: the hotspots for multifarious diseases in alzheimer's development
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335350/
https://www.ncbi.nlm.nih.gov/pubmed/30686983
http://dx.doi.org/10.3389/fnins.2018.01017
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