Parkinson’s Disease is the most prevalent neurodegenerative movement disorder, and is characterized by the progressive degeneration of dopaminergic neurons. However, increasing evidence also shows a conspicuous glial reaction together with neuro-inflammatory processes in Parkinson’s disease.
Recent data suggest neuroprotective activities of PEA in animal models of Parkinson’s disease. In particular, chronic treatment with PEA protects against loss of tyrosine hydroxylas- positive neurons in the substantia nigra pars compacta induced by the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, as well as toxin-induced microglial activation.
30 patients with advanced Parkinson’s disease, were treated with PEA and evaluated over a period of 12 months. In particular, each patient had taken the same L-dopa therapy without any modification for at least 4 consecutive weeks. Moreover, all patients were also evaluated at the time T0 (basal time), T1 (one month after T0), T3 (three months after T0), T6 (six months after T0) and T12 (one year after T0).
Patients received a daily dose of 1200 mg PEA for at least 3 months, followed by a dose reduction during 12 months.
All data were analyzed using a repeated measures analysis of variance (ANOVA).
Results: At the end of the follow up period analysis showed a statistically significant improvement (P<0,0001) of all the parameters considered, motor- and non-motor symptoms.
Furthermore, a significant reduction of dyskinesias and prolonged therapeutic effect of L-dopa therapy was seen.
PEA thus might play an important role in the pharmacological treatment of Parkinson’s disease by modulating the interaction between the dopaminergic pathways and glia.
Study conducted by Drs S. Brotini and L. Guidi, from the Movement Disorder Center, Department of Neurology, San Giuseppe Hospital, Empoli, Florence, Italy. LBA 21 from Late-BreakingStudyGroupAbstractsPublicationParkinson-Palmitoylethanolamide18th int congress on Parkinson’s disease, 2014.