ReviewNPJ aging and mechanisms of disease2015
The mammalian target of rapamycin at the crossroad between cognitive aging and Alzheimer's disease.
Review in NPJ aging and mechanisms of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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.
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.
Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- Presenilin-1 controls glycolysis and identity of pancreatic beta cells.Communications biology · 2026Article
- Unlocking the aging brain: mTORC1 as a convergent integrator for neurodegeneration and therapeutic intervention.Biogerontology · 2026Review
- Impact of sodium-glucose cotransporter-2 inhibitors on aging biomarkers and plasma ceramide levels in type 2 diabetes: beyond glycemic control.Annals of medicine · 2025Article
- PF-04691502, a PI3K/mTOR Dual Inhibitor, Ameliorates AD-like Pathology in a Mouse Model of AD.Cells · 2025Article
- Fasting is required for many of the benefits of calorie restriction in the 3xTg mouse model of Alzheimer's disease.Nature communications · 2025Article
- The Role of S6K1 in Aging and Alzheimer's Disease: Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Exploring the Mechanisms and Therapeutic Approaches of Mitochondrial Dysfunction in Alzheimer's Disease: An Educational Literature Review.Molecular neurobiology · 2025Review
- Mitochondrial One-Carbon Metabolism and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- PDIA3 Expression Is Altered in the Limbic Brain Regions of Triple-Transgenic Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Cannabis in Adolescence: Lasting Cognitive Alterations and Underlying Mechanisms.Cannabis and cannabinoid research · 2023Review
- Impaired autophagy in amyloid-beta pathology: A traditional review of recent Alzheimer's research.Journal of biomedical research · 2022Article
- Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Rapamycin Attenuated Zinc-Induced Tau Phosphorylation and Oxidative Stress in Rats: Involvement of Dual mTOR/p70S6K and Nrf2/HO-1 Pathways.Frontiers in immunology · 2022Article
- Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.Matrix biology plus · 2021Review
- Cancer-related cognitive impairment is associated with perturbations in inflammatory pathways.Cytokine · 2021Article
- Chemical and Structural Strategies to Selectively Target mTOR Kinase.ChemMedChem · 2021Review
- Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration.Molecular neurodegeneration · 2021Review
- mTOR in Alzheimer disease and its earlier stages: Links to oxidative damage in the progression of this dementing disorder.Free radical biology & medicine · 2021Review
- Systemic Actions of SGLT2 Inhibition on Chronic mTOR Activation as a Shared Pathogenic Mechanism between Alzheimer's Disease and Diabetes.Biomedicines · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-dependent cognitive decline is a major debilitating event affecting even individuals who are otherwise healthy. Understanding the molecular basis underlying these changes may increase the healthspan of the elderly population. It may also reveal insights into the pathogenesis of numerous neurodegenerative disorders characterized by cognitive deficits, as aging is the major risk factor for most of these disorders. Alzheimer's disease (AD), the most common neurodegenerative disorder, first manifests itself as deficits in encoding new memories. As AD progresses, these deficits spread to other cognitive domains that further debilitate the person before contributing to their demise. Suppression of the mammalian target of rapamycin (mTOR) increases healthspan and lifespan in several organisms. Numerous reports have linked alterations in mTOR signaling to age-dependent cognitive decline and the pathogenesis of AD. This review will discuss recent work highlighting the complex role of mTOR in cognitive aging and in the pathogenesis of AD.
Identifiers
What OpenQuestion holds
Registered trials
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.