N-Acylethanolamine Acid Amidase contributes to disease progression in a mouse model of multiple sclerosis
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Mice with experimental autoimmune encephalomyelitis (EAE), NAAA knockout mice, and a new line overexpressing NAAA in CD11b-positive myeloid cells (numbers not stated in the abstract)
- Dose used in the study
- No palmitoylethanolamide was given; NAAA was deleted or overexpressed genetically
- Duration
- Not stated in the abstract
- What was measured
- NAAA expression in spinal cord across disease stages and cell types; EAE onset and severity; alveolar macrophage iNOS and morphology; lung leukocyte response to intranasal lipopolysaccharide
What the authors reported
This laboratory study found:
- NAAA expression rose in spinal cord as EAE progressed, spreading from motor neurons and oligodendrocytes to microglia and macrophages.
- Genetic NAAA deletion delayed onset and reduced symptoms in female mice.
- Mice overexpressing NAAA in myeloid cells had activated macrophages with more iNOS, greater leukocyte accumulation after LPS, and more severe EAE than littermates.
Limits of this study
A mouse model of multiple sclerosis using genetic manipulation; it cannot show effect in people. PEA itself was not administered. Funding and conflicts not stated in the abstract, though Daniele Piomelli holds NAAA inhibitor patents noted in related papers.
Source
PubMed 32634582 · doi:10.1016/j.phrs.2020.105064
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.