ArticleFrontiers in neurology2018
Inhibition of mTORC1 Signaling Reverts Cognitive and Affective Deficits in a Mouse Model of Parkinson's Disease.
Article in Frontiers in neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Challenges and Opportunities in Exploring Non-Motor Symptoms in 6-Hydroxydopamine Models of Parkinson's Disease: A Systematic Review.Journal of neurochemistry · 2025Pooled it
- RNF168 dephosphorylation ameliorates cognitive decline in Aβ-based mouse models of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- CHCHD2 p.Thr61Ile knock-in mice exhibit motor defects and neuropathological features of Parkinson's disease.Brain pathology (Zurich, Switzerland) · 2023Article
- Herbal/Natural Compounds Resist Hallmarks of Brain Aging: From Molecular Mechanisms to Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Therapeutic Approaches to Non-Motor Symptoms of Parkinson's Disease: A Current Update on Preclinical Evidence.Current neuropharmacology · 2023Article
- Crosstalk of organelles in Parkinson's disease - MiT family transcription factors as central players in signaling pathways connecting mitochondria and lysosomes.Molecular neurodegeneration · 2022Review
- Protein clearance strategies for disease intervention.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Targeted activation of midbrain neurons restores locomotor function in mouse models of parkinsonism.Nature communications · 2022Article
- Dopamine activity on the perceptual salience for recognition memory.Frontiers in behavioral neuroscience · 2022Review
- Application of Neurotoxin-Induced Animal Models in the Study of Parkinson's Disease-Related Depression: Profile and Proposal.Frontiers in aging neuroscience · 2022Review
- The Emerging Roles of Autophagy in Human Diseases.Biomedicines · 2021Review
- mTOR Knockdown in the Infralimbic Cortex Evokes A Depressive-like State in Mouse.International journal of molecular sciences · 2021Article
- Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration.Molecular neurodegeneration · 2021Review
- Effect of rapamycin on aging and age-related diseases-past and future.GeroScience · 2021Review
- A Guide to the Generation of a 6-Hydroxydopamine Mouse Model of Parkinson's Disease for the Study of Non-Motor Symptoms.Biomedicines · 2021Article
- Inhibition of mTOR signaling by genetic removal of p70 S6 kinase 1 increases anxiety-like behavior in mice.Translational psychiatry · 2021Article
- Cellular Bioenergetics and AMPK and TORC1 Signalling in Blood Lymphoblasts Are Biomarkers of Clinical Status in FMR1 Premutation Carriers.Frontiers in psychiatry · 2021Article
- Compounds that extend longevity are protective in neurodegenerative diseases and provide a novel treatment strategy for these devastating disorders.Mechanisms of ageing and development · 2020Review
- Translation Regulation by eIF2α Phosphorylation and mTORC1 Signaling Pathways in Non-Communicable Diseases (NCDs).International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-motor symptoms, including cognitive deficits and affective disorders, are frequently diagnosed in Parkinson's disease (PD) patients and are only partially alleviated by dopamine replacement therapy. Here, we used a 6-hydroxydopamine (6-OHDA) mouse model of PD to examine the effects exerted on non-motor symptoms by inhibition of the mammalian target of rapamycin complex 1 (mTORC1), which is involved in the control of protein synthesis, cell growth, and metabolism. We show that rapamycin, which acts as an allosteric inhibitor of mTORC1, counteracts the impairment of novel object recognition. A similar effect is produced by PF-4708671, an inhibitor of the downstream target of mTORC1, ribosomal protein S6 kinase (S6K). Rapamycin is also able to reduce depression-like behavior in PD mice, as indicated by decreased immobility in the forced swim test. Moreover, rapamycin exerts anxiolytic effects, thereby reducing thigmotaxis in the open field and increasing exploration of the open arm in the elevated plus maze. In contrast to rapamycin, administration of PF-4708671 to PD mice does not counteract depression- and anxiety-like behaviors. Altogether, these results identify mTORC1 as a target for the development of drugs that, in combination with standard antiparkinsonian agents, may widen the efficacy of current therapies for the cognitive and affective symptoms of PD.
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