ArticlePharmacological research2022
Targeting NAAA counters dopamine neuron loss and symptom progression in mouse models of parkinsonism.
Article in Pharmacological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Causal effects of brain subregion gene expression on inflammatory bowel diseases revealed by Mendelian randomization and single cell analysis.Scientific reports · 2025Article
- The influence of genetics on the endocannabinoid system gene expression and relevance for targeting reproductive conditions.Journal of cannabis research · 2025Article
- Clinical and Metabolic Signatures ofKidney international reports · 2025Article
- Targeting microglial NAAA-regulated PEA signaling counters inflammatory damage and symptom progression of post-stroke anxiety.Cell communication and signaling : CCS · 2025Article
- Microbiome and metabolome integrated analysis: exploring potential diagnostic approaches for Parkinson's disease using tongue coating samples.Frontiers in microbiology · 2025Article
- N-acylethanolamine acid amidase inhibitor-loaded polymeric micelles in the treatment of dry eye disease.International journal of ophthalmology · 2025Article
- NAAA-regulated lipid signaling in monocytes controls the induction of hyperalgesic priming in mice.Nature communications · 2024Article
- Potential Neuroprotective Effect of the Endocannabinoid System on Parkinson's Disease.Parkinson's disease · 2024Review
- Goods and Bads of the Endocannabinoid System as a Therapeutic Target: Lessons Learned after 30 Years.Pharmacological reviews · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The lysosomal cysteine hydrolase N-acylethanolamine acid amidase (NAAA) deactivates palmitoylethanolamide (PEA), a lipid-derived PPAR-α agonist that is critically involved in the control of pain and inflammation. In this study, we asked whether NAAA-regulated PEA signaling might contribute to dopamine neuron degeneration and parkinsonism induced by the mitochondrial neurotoxins, 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In vitro experiments showed that 6-OHDA and MPTP enhanced NAAA expression and lowered PEA content in human SH-SY5Y cells. A similar effect was observed in mouse midbrain dopamine neurons following intra-striatal 6-OHDA injection. Importantly, deletion of the Naaa gene or pharmacological inhibition of NAAA activity substantially attenuated both dopamine neuron death and parkinsonian symptoms in mice treated with 6-OHDA or MPTP. Moreover, NAAA expression was elevated in postmortem brain cortex and premortem blood-derived exosomes from persons with Parkinson's disease compared to age-matched controls. The results identify NAAA-regulated PEA signaling as a molecular control point for dopaminergic neuron survival and a potential target for neuroprotective intervention.
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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.