ReviewNeurochemical research2016
AMPK Signalling and Defective Energy Metabolism in Amyotrophic Lateral Sclerosis.
Review in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled 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.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Environmental risk factors, protective factors, and biomarkers for amyotrophic lateral sclerosis: an umbrella review.Frontiers in aging neuroscience · 2025Pooled it
- Conserved NT5C2 links context-specific behaviors with psychiatric and metabolic risk.Behavioral and brain functions : BBF · 2026Article
- The GRK2/AP-1 Signaling Axis Mediates Vascular Endothelial Dysfunction and Atherosclerosis Induced by Oscillatory Low Shear Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mapping the Evidence for Measuring Energy Expenditure and Indicating Hypermetabolism in Motor Neuron Disease: A Scoping Review.Nutrition reviews · 2025Article
- Sephin1 suppresses ER stress-induced cell death by inhibiting the formation of PP2A holoenzyme.Cell death & disease · 2025Article
- CK and LRRK2 Involvement in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Trimetazidine Improves Mitochondrial Dysfunction in SOD1International journal of molecular sciences · 2024Article
- Microglial Metabolic Reprogramming: Emerging Insights and Therapeutic Strategies in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2023Review
- Article
- Distinct Plasma Immune Profile in ALS Implicates sTNFR-II in pAMPK/Leptin Homeostasis.International journal of molecular sciences · 2023Article
- αInternational journal of molecular sciences · 2023Review
- Metabolic Dysfunction in Motor Neuron Disease: Shedding Light through the Lens of Autophagy.Metabolites · 2022Review
- Characterization of the p.L145F and p.S135N Mutations in SOD1: Impact on the Metabolism of Fibroblasts Derived from Amyotrophic Lateral Sclerosis Patients.Antioxidants (Basel, Switzerland) · 2022Article
- Defects of Nutrient Signaling and Autophagy in Neurodegeneration.Frontiers in cell and developmental biology · 2022Review
- Immune Signaling Kinases in Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD).International journal of molecular sciences · 2021Review
- Neuroprotective Potential of Mild Uncoupling in Mitochondria. Pros and Cons.Brain sciences · 2021Review
- Metabolic Aspects of Adenosine Functions in the Brain.Frontiers in pharmacology · 2021Review
- Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration.International journal of molecular sciences · 2020Review
- A multistationary loop model of ALS unveils critical molecular interactions involving mitochondria and glucose metabolism.PloS one · 2020Article
- Why TDP-43? Why Not? Mechanisms of Metabolic Dysfunction in Amyotrophic Lateral Sclerosis.Neuroscience insights · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is caused by selective loss of upper and lower motor neurons by complex mechanisms that are incompletely understood. Motor neurons are large, highly polarised and excitable cells with unusually high energetic demands to maintain resting membrane potential and propagate action potentials. This leads to higher ATP consumption and mitochondrial metabolism in motor neurons relative to other cells. Here, we review increasing evidence that defective energy metabolism and homeostasis contributes to selective vulnerability and degeneration of motor neurons in ALS. Firstly, we provide a brief overview of major energetic pathways in the CNS, including glycolysis, oxidative phosphorylation and the AMP-activated protein kinase (AMPK) signalling pathway, while highlighting critical metabolic interactions between neurons and astrocytes. Next, we review evidence from ALS patients and transgenic mutant SOD1 mice for weight loss, hypermetabolism, hyperlipidemia and mitochondrial dysfunction in disease onset and progression. Genetic and therapeutic modifiers of energy metabolism in mutant SOD1 mice will also be summarised. We also present evidence that additional ALS-linked proteins, TDP-43 and FUS, lead to energy disruption and mitochondrial defects in motor neurons. Lastly, we review emerging evidence including our own that dysregulation of the AMPK signalling cascade in motor neurons is an early and common event in ALS pathogenesis. We suggest that an imbalance in energy metabolism should be considered an important factor in both progression and potential treatment of ALS.
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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.