ArticleMolecular neurodegeneration2017
Modulating the catalytic activity of AMPK has neuroprotective effects against α-synuclein toxicity.
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- A review on the relationship between the distal 1q21.1 microdeletion and schizophrenia.Frontiers in genetics · 2025Review
- AMPK: The energy sensor at the crossroads of aging and cancer.Seminars in cancer biology · 2024Review
- Function and Mechanism of Abscisic Acid on Microglia-Induced Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Olfactory dysfunction as an early pathogenic indicator inFrontiers in aging neuroscience · 2024Article
- Stable isotope labeling and ultra-high-resolution NanoSIMS imaging reveal alpha-synuclein-induced changes in neuronal metabolism in vivo.Acta neuropathologica communications · 2023Article
- Oleuropein confers neuroprotection against rotenone-induced model of Parkinson's disease via BDNF/CREB/Akt pathway.Scientific reports · 2023Article
- Genetic modifiers of synucleinopathies-lessons from experimental models.Oxford open neuroscience · 2023Review
- Methanolic Extract of Boswellia serrata Gum Protects the Nigral Dopaminergic Neurons from Rotenone-Induced Neurotoxicity.Molecular neurobiology · 2022Article
- Metformin and Dementia Risk: A Systematic Review with Respect to Time Related Biases.Journal of Alzheimer's disease reports · 2022Article
- Korean Red Ginseng Improves Astrocytic Mitochondrial Function by Upregulating HO-1-Mediated AMPKα-PGC-1α-ERRα Circuit after Traumatic Brain Injury.International journal of molecular sciences · 2021Article
- Targeting autophagy using small-molecule compounds to improve potential therapy of Parkinson's disease.Acta pharmaceutica Sinica. B · 2021Review
- Adiponectin-mimetic novel nonapeptide rescues aberrant neuronal metabolic-associated memory deficits in Alzheimer's disease.Molecular neurodegeneration · 2021Article
- Build-UPS and break-downs: metabolism impacts on proteostasis and aging.Cell death and differentiation · 2021Review
- "Janus-Faced" α-Synuclein: Role in Parkinson's Disease.Frontiers in cell and developmental biology · 2021Review
- Dietary Amino Acids Impact LRRK2-Induced Neurodegeneration in Parkinson's Disease Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Nano-imaging trace elements at organelle levels in substantia nigra overexpressing α-synuclein to model Parkinson's disease.Communications biology · 2020Article
- P2X7 Receptor is Involved in Mitochondrial Dysfunction Induced by Extracellular Alpha Synuclein in Neuroblastoma SH-SY5Y Cells.International journal of molecular sciences · 2020Article
- FGF21 Protects Dopaminergic Neurons in Parkinson's Disease Models Via Repression of Neuroinflammation.Neurotoxicity research · 2020Article
- Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway.Molecular neurodegeneration · 2020Article
- Autophagy activation promotes clearance of α-synuclein inclusions in fibril-seeded human neural cells.The Journal of biological chemistry · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetabolic perturbations and slower renewal of cellular components associated with aging increase the risk of Parkinson's disease (PD). Declining activity of AMPK, a critical cellular energy sensor, may therefore contribute to neurodegeneration.
methodsHere, we overexpress various genetic variants of the catalytic AMPKα subunit to determine how AMPK activity affects the survival and function of neurons overexpressing human α-synuclein in vivo.
resultsBoth AMPKα1 and α2 subunits have neuroprotective effects against human α-synuclein toxicity in nigral dopaminergic neurons. Remarkably, a modified variant of AMPKα1 (T172Dα1) with constitutive low activity most effectively prevents the loss of dopamine neurons, as well as the motor impairments caused by α-synuclein accumulation. In the striatum, T172Dα1 decreases the formation of dystrophic axons, which contain aggregated α-synuclein. In primary cortical neurons, overexpression of human α-synuclein perturbs mitochondrial and lysosomal activities. Co-expressing AMPKα with α-synuclein induces compensatory changes, which limit the accumulation of lysosomal material and increase the mitochondrial mass.
conclusionsTogether, these results indicate that modulating AMPK activity can mitigate α-synuclein toxicity in nigral dopamine neurons, which may have implications for the development of neuroprotective treatments against PD.
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