ReviewAnatomy & cell biology2016
The association between PGC-1α and Alzheimer's disease.
Review in Anatomy & cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 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
51 citing papers in PubMed.
- A Lipoylation-PDH-TCA Transcriptional Deficit in the Alzheimer's Disease Cortex - Donor-level Multi-cohort Evidence with Neuronal-composition, Disease-specificity and Matched-null Controls.Journal of molecular neuroscience : MN · 2026Article
- Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch.Frontiers in aging neuroscience · 2026Article
- Liuwei Dihuang pills attenuates cognitive dysfunction inFrontiers in pharmacology · 2026Article
- Bridging the molecular and clinical aspects of resveratrol in Alzheimer's disease: a review.3 Biotech · 2025Review
- Article
- Combined exercise and Hawthorn protect against learning impairments and hippocampal damage from trimethyltin neurotoxicity in rat.Scientific reports · 2025Article
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Mechanism study of exercise intervention on circadian disruption in Alzheimer's disease.Frontiers in neuroscience · 2025Review
- The Protective Effects of Syringic Acid on Bisphenol A-Induced Neurotoxicity Possibly Through AMPK/PGC-1α/Fndc5 and CREB/BDNF Signaling Pathways.Molecular neurobiology · 2024Article
- Review
- A single-cell and spatial RNA-seq database for Alzheimer's disease (ssREAD).Nature communications · 2024Article
- A Single-cell and Spatial RNA-seq Database for Alzheimer's Disease (ssREAD).bioRxiv : the preprint server for biology · 2024Article
- Effects of Dietary Restriction on PGC-1α Regulation in the Development of Age-associated Diseases.Current aging science · 2024Review
- Article
- Exercise modulates APOE expression in brain cortex of female APOE3 and APOE4 targeted replacement mice.Neuropeptides · 2023Article
- Tanshinone IIA ameliorates Aβ transendothelial transportation through SIRT1-mediated endoplasmic reticulum stress.Journal of translational medicine · 2023Article
- The Novel Role of Mitochondrial Citrate Synthase and Citrate in the Pathophysiology of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- E2F4DN Transgenic Mice: A Tool for the Evaluation of E2F4 as a Therapeutic Target in Neuropathology and Brain Aging.International journal of molecular sciences · 2022Review
- Effects of an Exercise Program Combining Aerobic and Resistance Training on Protein Expressions of Neurotrophic Factors in Obese Rats Injected with Beta-Amyloid.International journal of environmental research and public health · 2022Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder and its reported pathophysiological features in the brain include the deposition of amyloid beta peptide, chronic inflammation, and cognitive impairment. The incidence of AD is increasing worldwide and researchers have studied various aspects of AD pathophysiology in order to improve our understanding of the disease. Thus far, the onset mechanisms and means of preventing AD are completely unknown. Peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) is a protein related to various cellular mechanisms that lead to the alteration of downstream gene regulation. It has been reported that PGC-1α could protect cells against oxidative stress and reduce mitochondrial dysfunction. Moreover, it has been demonstrated to have a regulatory role in inflammatory signaling and insulin sensitivity related to cognitive function. Here, we present further evidence of the involvement of PGC-1α in AD pathogenesis. Clarifying the relationship between PGC-1α and AD pathology might highlight PGC-1α as a possible target for therapeutic intervention in AD.
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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.