हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।
ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं
Olivola Enrica, Cerroni Rocco, Conti Marco, Pierantozzi Mariangela, Liguori Claudio and Stefani Alessandro
Objective: Several investigations have recently inferred that a low serum vitamin D concentration may contribute to cognitive impairment in the elderly. Here, we assessed whether in a cohort of Parkinson’s disease (PD) patients attributable to any disease stage a deficit in serum 25-hydroxyvitamin D (25(OH) D) levels occurred as previously proposed and, more importantly, if it is correlated with cognitive impairment or disease duration. Methods: Our PD group (n=54) was compared to an age-matched control group (n= 30), but also to patients afflicted by Alzheimer’s disease (AD) (n= 17) and motor neuron disease (amyotrophic lateral sclerosis - ALS) (n=19). Results: Serum 25(OH)D levels > 30 ng/ml was found in 37% of PD patients (versus 76% in controls); in 34 out of 54 PD patients low 25(OH)D levels occurred (28,73 ± 20,22 ng/ml vs 44,52 ± 18,48 ng/ml in control group); however, no correlation with mini mental state examination (MMSE) or disease progression emerged in PD patients. AD cohort was characterized by a significantly lower vitamin D concentration (half manifesting severe deficiency below 10 ng/ml, in contrast with 18% amongst PD). To note, also in ALS, pathological low levels of vitamin D, comparable to PD, was found. Conclusion: Our findings highlight that vitamin D insufficiency or deficiency is shared by multiple neurodegenerative diseases, albeit a-specifically. In PD, 25(OH) D levels do not correlate with cognitive performance. On one hand, these data confirm the opportunity to restore vitamin D levels in a variety of neurological disorders; on the other, they suggest that, in PD, at contrast with AD, vitamin D insufficiency should not play a relevant role in influencing disease severity or unmasking an associated dementia.