👤 Elzbieta Buczek

Glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) are proteins essential for neuronal survival and implicated in Parkinson's disease (PD) pathophysiology. Although reduced levels of these neurotrophins have been observed in PD, their relationship with disease progression remains unclear. We conducted a systematic review by independently searching four databases using predefined keywords: Parkinson AND (GDNF OR BDNF OR neurotroph) AND (serum OR blood OR cerebrospinal fluid). After screening 2132 records, 35 studies qualified for inclusion. Changes in neurotrophic factors' levels were evaluated in relation to disease severity and duration. Many studies reported a decline in BDNF levels associated with more severe motor symptoms. Some studies noted increased BDNF levels in advanced PD. This pattern may be affected by levodopa treatment, suggesting that elevated BDNF levels in advanced PD could reflect a treatment-related effect rather than disease progression itself. Reduced levels of both GDNF and BDNF were linked to cognitive decline, with BDNF also decreased in PD patients with depression. Serum BDNF levels were associated with motor severity and neuropsychiatric symptoms. BDNF levels in PD may increase with longer disease duration, likely due to levodopa treatment effects. However, lower BDNF levels are seen in cognitive decline and depression, frequent non-motor symptoms of PD. Further research is required to clarify BDNF dynamics and to determine GDNF's role in motor progression and cognitive decline. Show less

While the plasma phylloquinone (PK) concentration is inversely correlated with cardiovascular risk, the involvement of PK in regulating endothelial function has not been directly investigated. Therefore, in this study we assessed the effects of short-term treatment with PK-deficient diets (5-10 weeks) on endothelial function in normolipidemic 14-week-old male C57BL/6JCmd mice and age-matched dyslipidaemic male E3L.CETP mice. Our results show that in normolipidemic mice dietary PK deficiency was associated with a marked reduction of PK levels in the plasma and liver (liquid chromatography-mass spectrometry measurements) and with impaired endothelium-dependent vasodilation assessed in vivo by magnetic resonance imaging (MRI). Dietary PK deficiency-induced endothelial dysfunction was fully reversed by PK supplementation. In dyslipidaemic E3L.CETP mice, dietary PK deficiency exacerbated preexisting endothelial dysfunction. Furthermore, dietary PK deficiency decreased menaquinone-4 (MK-4) levels in the aorta but did not affect blood coagulation (calibrated automated thrombography), microbiota composition (culturing and next-generation sequencing), and gut menaquinone production. In conclusion, our study demonstrated for the first time that sufficient dietary PK intake supports endothelial function in normolipidemic and dyslipidaemic mice indicating nutritional significance of dietary PK in the maintenance of endothelial function in humans. Show less