Evidence map›Paper›PMID 33933601›Full record

ReviewFree radical biology & medicine2021

mTOR in Alzheimer disease and its earlier stages: Links to oxidative damage in the progression of this dementing disorder.

M Perluigi, F Di Domenico, E Barone, D A Butterfield

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 115 citations in OpenAlex.

  1. mTORC2-NaChannels (Austin, Tex.) · 2026
    Article
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  4. Blood-based proteomic signature of amyloidosis: identification of novel regulators of amyloid load.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  17. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  18. Review
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 2 countries.

M PerluigiDepartment of Biochemical Sciences "A. Rossi-Fanelli", Sapienza University of Rome, Piazzale A. Moro 5, 00185, Roma, Italy.
F Di DomenicoDepartment of Biochemical Sciences "A. Rossi-Fanelli", Sapienza University of Rome, Piazzale A. Moro 5, 00185, Roma, Italy.
E BaroneDepartment of Biochemical Sciences "A. Rossi-Fanelli", Sapienza University of Rome, Piazzale A. Moro 5, 00185, Roma, Italy.
D A ButterfieldDepartment of Chemistry, Sapienza University of Rome, Piazzale A. Moro 5, 00185, Roma, Italy; Department of Chemistry and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, 40506-0055, USA. Electronic address: dabcns@uky.edu.
Sapienza University of Rome · IT

Funding

APOE and the PPP: Glucose Metabolism and Oxidative Stress in Alzheimer's DiseaseR01AG060056 · NIA · UNIVERSITY OF KENTUCKY · PI JOHNSON, LANCE ALLEN · 2018 to 2022
$2.5M
mTOR activation and the pathogenesis of Alzheimer disease in Down syndromeR56AG055596 · NIA · UNIVERSITY OF KENTUCKY · PI BUTTERFIELD, D. ALLAN, HEAD, ELIZABETH · 2018 to 2018
$566k
NIA NIH HHS R01 AG060056NIA NIH HHS R56 AG055596
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population and has worldwide impact. The etiology of the disease is complex and results from the confluence of multiple mechanisms ultimately leading to neuronal loss and cognitive decline. Among risk factors, aging is the most relevant and accounts for several pathogenic events that contribute to disease-specific toxic mechanisms. Accumulating evidence linked the alterations of the mammalian target of rapamycin (mTOR), a serine/threonine protein kinase playing a key role in the regulation of protein synthesis and degradation, to age-dependent cognitive decline and pathogenesis of AD. To date, growing studies demonstrated that aberrant mTOR signaling in the brain affects several pathways involved in energy metabolism, cell growth, mitochondrial function and proteostasis. Recent advances associated alterations of the mTOR pathway with the increased oxidative stress. Disruption of all these events strongly contribute to age-related cognitive decline including AD. The current review discusses the main regulatory roles of mTOR signaling network in the brain, focusing on its role in autophagy, oxidative stress and energy metabolism. Collectively, experimental data suggest that targeting mTOR in the CNS can be a valuable strategy to prevent/slow the progression of AD.

Indexed as

Alzheimer DiseaseAgedAutophagyHumansOxidative StressSignal TransductionTOR Serine-Threonine KinasesMTOR protein, humanTOR Serine-Threonine KinasesAlzheimer's diseasemTOROxidative stressProtein aggregationProteostasis

Identifiers

PMID33933601
PMCPMC8145782
OpenAlexW3159355990

What OpenQuestion holds

Textmetadata
LicenceTDM
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.