Palmitoylethanolamide counteracts brain fog improving depressive-like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Male C57Bl/6J mice made obese with 12 weeks of high-fat diet (HFD), then treated for a further 7 weeks alongside continued HFD
- Dose used in the study
- Ultra-micronised PEA, 30 mg/kg daily, oral
- Duration
- 7 weeks of treatment, following 12 weeks of high-fat diet
- What was measured
- Depressive- and anhedonic-like behaviour, cognitive performance, monoamine levels in nucleus accumbens/prefrontal cortex/hippocampus, and markers of synaptic plasticity and neurogenesis in hippocampus
What the authors reported
The study found:
- PEA reduced depressive- and anhedonic-like behaviour and cognitive deficits caused by the high-fat diet.
- It raised serotonin in prefrontal cortex, reduced dopamine and serotonin turnover in the nucleus accumbens and prefrontal cortex, and raised dopamine in hippocampus and prefrontal cortex.
- PEA also restored BDNF signalling and glutamatergic synaptic density in the hippocampus and promoted neurogenesis.
Limits of this study
A diet-induced obesity mouse model; it cannot show effect in people. Funding and conflicts not stated in the abstract.
Source
PubMed 32346865 · doi:10.1111/bph.15071
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.