Targeting NAAA counters dopamine neuron loss and symptom progression in mouse models of parkinsonism
Laboratory studyHumansOther animalsWith NAAA gene deletion or NAAA inhibitors, which raise the body's own palmitoylethanolamide; PEA itself was not given
This study tested palmitoylethanolamide together with NAAA gene deletion or NAAA inhibitors, which raise the body's own palmitoylethanolamide; PEA itself was not given. Its results cannot be assigned to palmitoylethanolamide alone. More combination studies.
- Design
- Laboratory study
- Subjects
- Human SH-SY5Y cells; mice given 6-OHDA or MPTP; post-mortem brain cortex and blood exosomes from people with Parkinson's disease and age-matched controls
- Dose used in the study
- Not stated in the abstract
- Duration
- Not stated in the abstract
- What was measured
- NAAA expression and palmitoylethanolamide content in cells and mouse midbrain; dopamine neuron death and parkinsonian symptoms in mice; NAAA levels in human brain and blood samples
What the authors reported
The toxins raised NAAA and lowered PEA in cells and mouse dopamine neurons. Deleting the Naaa gene or inhibiting NAAA substantially reduced dopamine neuron death and parkinsonian symptoms in mice, and NAAA was higher in brain cortex and blood exosomes from people with Parkinson's disease than in controls.
Limits of this study
Mouse and cell work plus human tissue measurements; it cannot show effect in people treated in practice, and no palmitoylethanolamide was given. The senior author holds patents on NAAA inhibitors.
Source
PubMed 35781057 · doi:10.1016/j.phrs.2022.106338
Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.