ReviewProgress in neurobiology2012
PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington's disease to Parkinson's disease and beyond.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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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.
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Who cites it
64 citing papers in PubMed, 117 citations in OpenAlex.
- Creatine-weighted imaging in patients with Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Mitochondria-Mediated Mechanisms of Ferroptosis in Neurological Diseases.Neurochemical research · 2025Review
- Article
- Impaired Mitochondrial Function and Ubiquitin Proteasome System Activate α-Synuclein Aggregation in Zinc-Induced Neurotoxicity: Effect of Antioxidants.Journal of molecular neuroscience : MN · 2025Article
- Therapeutic potential of berries in age-related neurological disorders.Frontiers in pharmacology · 2024Review
- ATP13A2 activates the pentose phosphate pathway to promote colorectal cancer growth though TFEB-PGD axis.Clinical and translational medicine · 2023Article
- PGC-1α Affects Epileptic Seizures by Regulating Mitochondrial Fusion in Epileptic Rats.Neurochemical research · 2023Article
- Resveratrol Improves Paclitaxel-Induced Cognitive Impairment in Mice by Activating SIRT1/PGC-1α Pathway to Regulate Neuronal State and Microglia Cell Polarization.Drug design, development and therapy · 2023Article
- Metabolic Regulation of Mitochondrial Protein Biogenesis from a Neuronal Perspective.Biomolecules · 2022Review
- Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage.Molecules (Basel, Switzerland) · 2022Review
- Regulation of PGC1α Downstream of the Insulin Signaling Pathway Plays a Role in the Hepatic Proteotoxicity of Mutant α1-Antitrypsin Deficiency Variant Z.Gastroenterology · 2022Article
- Non-coding RNA in alcohol use disorder by affecting synaptic plasticity.Experimental brain research · 2022Review
- Deciphering the role of PGC-1α in neurological disorders: from mitochondrial dysfunction to synaptic failure.Neural regeneration research · 2022Review
- DNA Methylation: A Promising Approach in Management of Alzheimer's Disease and Other Neurodegenerative Disorders.Biology · 2022Review
- Mitochondrial Abnormalities and Synaptic Damage in Huntington's Disease: a Focus on Defective Mitophagy and Mitochondria-Targeted Therapeutics.Molecular neurobiology · 2021Review
- Flavonoids modulate AMPK/PGC-1α and interconnected pathways toward potential neuroprotective activities.Metabolic brain disease · 2021Review
- Regulation of neuronal bioenergetics as a therapeutic strategy in neurodegenerative diseases.Neural regeneration research · 2021Article
- A Balanced Act: The Effects of GH-GHR-IGF1 Axis on Mitochondrial Function.Frontiers in cell and developmental biology · 2021Review
- Peroxisome Proliferator-Activated Receptor γ Coactivator 1α Activates Vascular Endothelial Growth Factor That Protects Against Neuronal Cell Death Following Status Epilepticus through PI3K/AKT and MEK/ERK Signaling.International journal of molecular sciences · 2020Article
- Muscarinic Toxin 7 Signals Via CaMolecular neurobiology · 2020Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neurons are specialized cells with unique features, including a constant high demand for energy. Mitochondria satisfy this constant demand, and are emerging as a central target for dysfunction in neurodegenerative disorders, such as Huntington's disease (HD) and Parkinson's disease. PPARγ co-activator-1α (PGC-1α) is a transcription co-activator for nuclear receptors such as the PPARs, and thereby coordinates a number of gene expression programs to promote mitochondrial biogenesis and oxidative phosphorylation. Studies of PGC-1α knock-out mice have yielded important insights into the role of PGC-1α in normal nervous system function and potentially neurological disease. HD is caused by a polyglutamine repeat expansion in the huntingtin protein, and decades of work have established mitochondrial dysfunction as a key feature of HD pathogenesis. However, after the discovery of the HD gene, numerous reports produced strong evidence for altered transcription in HD. In 2006, a series of studies revealed that PGC-1α transcription interference contributes to HD neurodegeneration, linking the nuclear transcriptionopathy with the mitochondrial dysfunction. Subsequent work has strengthened this view, and further extended the role of PGC-1α within the CNS. Within the last year, studies of Parkinson's disease, another involuntary movement disorder long associated with mitochondrial dysfunction, have shown that PGC-1α dysregulation is contributing to its pathogenesis. As PGC-1α is likely also important for aging, a process with considerable relevance to neuron function, translational studies aimed at developing therapies based upon the PGC-1α pathway as a high priority target are underway.
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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.