ISSN: 2161-0460

Jornal da doença de Alzheimer e parkinsonismo

Acesso livre

Nosso grupo organiza mais de 3.000 Séries de conferências Eventos todos os anos nos EUA, Europa e outros países. Ásia com o apoio de mais 1.000 Sociedades e publica mais de 700 Acesso aberto Periódicos que contém mais de 50.000 personalidades eminentes, cientistas de renome como membros do conselho editorial.

Periódicos de acesso aberto ganhando mais leitores e citações
700 periódicos e 15 milhões de leitores Cada periódico está obtendo mais de 25.000 leitores

Indexado em
  • Índice Copérnico
  • Google Scholar
  • Sherpa Romeu
  • Abra o portão J
  • Genâmica JournalSeek
  • Chaves Acadêmicas
  • JornalTOCs
  • Infraestrutura Nacional de Conhecimento da China (CNKI)
  • Biblioteca de Periódicos Eletrônicos
  • RefSeek
  • Universidade Hamdard
  • EBSCO AZ
  • OCLC – WorldCat
  • Catálogo online SWB
  • Biblioteca Virtual de Biologia (vifabio)
  • Publons
  • Fundação de Genebra para Educação e Pesquisa Médica
  • Euro Pub
  • ICMJE
Compartilhe esta página

Abstrato

Low Serum 25(OH)D Levels in Parkinson Disease; a Non Specific Marker of Neurodegeneration?

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.