ABSTRACT
JOURNAL/nrgr/04.03/01300535-202502000-00033/figure1/v/2024-05-28T214302Z/r/image-tiff There is a need to develop interventions to slow or reverse the degeneration of dopamine neurons in Parkinson's disease after diagnosis. Given that preclinical and clinical studies suggest benefits of dietary n-3 polyunsaturated fatty acids, such as docosahexaenoic acid, and exercise in Parkinson's disease, we investigated whether both could synergistically interact to induce recovery of the dopaminergic pathway. First, mice received a unilateral stereotactic injection of 6-hydroxydopamine into the striatum to establish an animal model of nigrostriatal denervation. Four weeks after lesion, animals were fed a docosahexaenoic acid-enriched or a control diet for the next 8 weeks. During this period, the animals had access to a running wheel, which they could use or not. Docosahexaenoic acid treatment, voluntary exercise, or the combination of both had no effect on (i) distance traveled in the open field test, (ii) the percentage of contraversive rotations in the apomorphine-induction test or (iii) the number of tyrosine-hydroxylase-positive cells in the substantia nigra pars compacta. However, the docosahexaenoic acid diet increased the number of tyrosine-hydroxylase-positive terminals and induced a rise in dopamine concentrations in the lesioned striatum. Compared to docosahexaenoic acid treatment or exercise alone, the combination of docosahexaenoic acid and exercise (i) improved forelimb balance in the stepping test, (ii) decreased the striatal DOPAC/dopamine ratio and (iii) led to increased dopamine transporter levels in the lesioned striatum. The present results suggest that the combination of exercise and docosahexaenoic acid may act synergistically in the striatum of mice with a unilateral lesion of the dopaminergic system and provide support for clinical trials combining nutrition and physical exercise in the treatment of Parkinson's disease.
ABSTRACT
OBJECTIVE: Docosahexaenoic acid (DHA) is vital for fetal development especially during the third trimester of gestation when the speed of fetal brain growth is at its peak. Diabetes modifies the maternal fatty acid profile, which may in turn change the quantity and/or quality of lipids transferred to the fetus. Neonates born to diabetic mothers might be more vulnerable to DHA deficiency leading to lower cognitive scores together with lower overall intellectual quotients when compared to control. We reviewed the influence of type 1 or type 2 pre-gestational (PGD) and gestational diabetes mellitus (GDM) on maternal and fetal DHA levels. METHOD: We searched MEDLINE articles about PGD and/or GDM and DHA published before October 2016. RESULTS: Maternal blood DHA level seems higher in those with diabetes than those without diabetes. However, DHA in cord plasma of neonates born to PGD and/or GDM mothers seem lower compared to neonates born to nondiabetic mothers. CONCLUSIONS: Altogether, these results suggest that the transfer of DHA from the mother to the fetus may be deficient or dysregulated in diabetic pregnancies. What remains to be understood is how placental lipid transport is regulated and whether there is a link with clinical neurodevelopmental phenotypes in the newborns.
