Evidence map›Paper›PMID 30686983›Full record

ReviewFrontiers in neuroscience2018

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

Zeba Mueed, Pallavi Tandon, Sanjeev Kumar Maurya, Ravi Deval, Mohammad A Kamal, Nitesh Kumar Poddar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 108 citations in OpenAlex.

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  13. Pathway enrichment in genome-wide analysis of longitudinal Alzheimer's disease biomarker endophenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  19. Inhalation exposure-induced toxicity and disease mediated via mTOR dysregulation.Experimental biology and medicine (Maywood, N.J.) · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Zeba MueedDepartment of Biotechnology, Invertis University, Bareilly, India.
Pallavi TandonDepartment of Biotechnology, Invertis University, Bareilly, India.
Sanjeev Kumar MauryaDepartment of Biotechnology, Invertis University, Bareilly, India.
Ravi DevalDepartment of Biotechnology, Invertis University, Bareilly, India.
Mohammad A KamalKing Fahad Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Nitesh Kumar PoddarDepartment of Biotechnology, Invertis University, Bareilly, India.
Invertis University · INKing Abdulaziz University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Alzheimer's disease (AD)Aβ modulatorsAβ plaqueshyperphosphorylationmTORNFT'stau

Identifiers

PMID30686983
PMCPMC6335350
OpenAlexW2910097122

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.