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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Main Authors: Zeba Mueed, Pallavi Tandon, Sanjeev Kumar Maurya, Ravi Deval, Mohammad A. Kamal, Nitesh Kumar Poddar
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-01-01
Series:Frontiers in Neuroscience
Subjects:
tau
Online Access:https://www.frontiersin.org/article/10.3389/fnins.2018.01017/full
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spelling doaj-24d49bab04cd4361a9afaef89ec093a62020-11-24T21:06:14ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2019-01-011210.3389/fnins.2018.01017371025Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's DevelopmentZeba Mueed0Pallavi Tandon1Sanjeev Kumar Maurya2Ravi Deval3Mohammad A. Kamal4Mohammad A. Kamal5Mohammad A. Kamal6Nitesh Kumar Poddar7Department of Biotechnology, Invertis University, Bareilly, IndiaDepartment of Biotechnology, Invertis University, Bareilly, IndiaDepartment of Biotechnology, Invertis University, Bareilly, IndiaDepartment of Biotechnology, Invertis University, Bareilly, IndiaKing Fahad Medical Research Center, King Abdulaziz University, Jeddah, Saudi ArabiaEnzymoics, Hebersham, NSW, AustraliaNovel Global Community Educational Foundation, Hebersham, NSW, AustraliaDepartment of Biotechnology, Invertis University, Bareilly, IndiaThe 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.https://www.frontiersin.org/article/10.3389/fnins.2018.01017/fullAlzheimer's disease (AD)taumTORAβ plaquesAβ modulatorshyperphosphorylation
collection DOAJ
language English
format Article
sources DOAJ
author Zeba Mueed
Pallavi Tandon
Sanjeev Kumar Maurya
Ravi Deval
Mohammad A. Kamal
Mohammad A. Kamal
Mohammad A. Kamal
Nitesh Kumar Poddar
spellingShingle Zeba Mueed
Pallavi Tandon
Sanjeev Kumar Maurya
Ravi Deval
Mohammad A. Kamal
Mohammad A. Kamal
Mohammad A. Kamal
Nitesh Kumar Poddar
Tau and mTOR: The Hotspots for Multifarious Diseases in Alzheimer's Development
Frontiers in Neuroscience
Alzheimer's disease (AD)
tau
mTOR
Aβ plaques
Aβ modulators
hyperphosphorylation
author_facet Zeba Mueed
Pallavi Tandon
Sanjeev Kumar Maurya
Ravi Deval
Mohammad A. Kamal
Mohammad A. Kamal
Mohammad A. Kamal
Nitesh Kumar Poddar
author_sort Zeba Mueed
title 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_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_sort tau and mtor: the hotspots for multifarious diseases in alzheimer's development
publisher Frontiers Media S.A.
series Frontiers in Neuroscience
issn 1662-453X
publishDate 2019-01-01
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.
topic Alzheimer's disease (AD)
tau
mTOR
Aβ plaques
Aβ modulators
hyperphosphorylation
url https://www.frontiersin.org/article/10.3389/fnins.2018.01017/full
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