Dataset Information

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact.

ABSTRACT: It is widely known that vitamin D receptors have been found in neurons and glial cells, and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. Vitamin D helps the regulation of neurotrophin, neural differentiation, and maturation, through the control operation of growing factors synthesis (i.e., neural growth factor [NGF] and glial cell line-derived growth factor (GDNF), the trafficking of the septohippocampal pathway, and the control of the synthesis process of different neuromodulators (such as acetylcholine [Ach], dopamine [DA], and gamma-aminobutyric [GABA]). Based on these assumptions, we have written this review to summarize the potential role of vitamin D in neurological pathologies. This work could be titanic and the results might have been very fuzzy and even incoherent had we not conjectured to taper our first intentions and devoted our interests towards three mainstreams, demyelinating pathologies, vascular syndromes, and neurodegeneration. As a result of the lack of useful therapeutic options, apart from the disease-modifying strategies, the role of different risk factors should be investigated in neurology, as their correction may lead to the improvement of the cerebral conditions. We have explored the relationships between the gene-environmental influence and long-term vitamin D deficiency, as a risk factor for the development of different types of neurological disorders, along with the role and the rationale of therapeutic trials with vitamin D implementation.

SUBMITTER: Moretti R

PROVIDER: S-EPMC6121649 | biostudies-other | 2018 Jul

REPOSITORIES: biostudies-other

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Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact.

Moretti Rita R Morelli Maria Elisa ME Caruso Paola P

International journal of molecular sciences 20180731 8

It is widely known that vitamin D receptors have been found in neurons and glial cells, and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. Vitamin D helps the regulation of neurotrophin, neural differentiation, and maturation, through the control operation of growing factors synthesis (i.e., neural growth factor [NGF] and glial cell line-derived growth factor (GDNF), the trafficking of the septohippocampal pathway, and th ...[more]

PMID: 30065237

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Project description:BackgroundNonadherence to medication contributes substantially to worse health outcomes. Especially among older adults with chronic illness, multimorbidity leads to complex medication regimes and high nonadherence rates. In previous research, depressive symptomology has been identified as a major contributor to nonadherence, and some authors hypothesize a link via motivational deficits and low self-efficacy. However, the exact mechanisms linking depressive symptomology and nonadherence are not yet understood. This is in part because the often-employed sum scores cannot do justice to the complexity of depressive symptomology; instead, it is recommended to assess the influence of individual symptoms.MethodsFollowing this symptom-based approach, we performed correlation, network and regression analysis using depressive symptoms as depicted by the items of the revised Beck Depression Inventory II (BDI) to assess their influence with nonadherence in N = 731 older adults with chronic neurological diseases. Nonadherence was measured with the self-report Stendal Adherence to Medication Score (SAMS).ResultsEven when controlling for sociodemographic and health-related covariates, the BDI remained the most influential contributor to nonadherence. Across different methods, Loss of Interest and Difficulty with Concentration were identified as particularly influential for nonadherence, linking nonadherence with other affective or somatic BDI items, respectively. Additionally, Fatigue, Problems with Decision Making, Suicidal Thoughts, and Worthlessness contribute to nonadherence.ConclusionUsing a symptom-driven approach, we aimed to understand which depressive symptoms contribute to higher levels of nonadherence. Our results refine previous hypotheses about motivation and control beliefs by suggesting that it is not merely a lack of beliefs in the efficacy of medication that connects depressive symptoms and nonadherence, but rather an overall lack of interest in improving one's health due to feelings of worthlessness and suicidal tendencies. This lack of interest is further substantiated by already sparse resources caused by changes in concentration and fatigue. In order to improve health outcomes and reduce nonadherence, these associations between depressive symptoms must be further understood and targeted in tailored interventions.

Project description:Microglia are the innate sentinels of the central nervous system (CNS) and are responsible for the homeostasis and immune defense of the CNS. Under the influence of the local environment and cell-cell interaction, microglia exhibit a multidimensional and context-dependent phenotypes that can be cytotoxic and neuroprotective. Recent studies suggest that microglia express multitudinous types of lectins, including galectins, Siglecs, mannose-binding lectins (MBLs) and other glycan binding proteins. Because most studies that examine lectins focus on the peripheral system, the functions of lectins have not been critically investigated in the CNS. In addition, the types of brain cells that contribute to the altered levels of lectins present in diseases are often unclear. In this review, we will discuss how galectins, Siglecs, selectins and MBLs contribute to the dynamic functions of microglia. The interacting ligands of these lectins are complex glycoconjugates, which consist of glycoproteins and glycolipids that are expressed on microglia or surrounding cells. The current understanding of the heterogeneity and functions of glycans in the brain is limited. Galectins are a group of pleotropic proteins that recognize both ?-galactoside-containing glycans and non- ?-galactoside-containing proteins. The function and regulation of galectins have been implicated in immunomodulation, neuroinflammation, apoptosis, phagocytosis and oxidative bursts. Most Siglecs are expressed at a low level on the plasma membrane and bind to sialic acid residues for immunosurveillance and cell-cell communication. Siglecs are classified based on their inhibitory and activatory downstream signaling properties. Inhibitory Siglecs negatively regulate microglia activation upon recognizing the intact sialic acid patterns and vice versa. MBLs are expressed upon infection in cytoplasm and can be secreted in order to recognize molecules containing terminal mannose as an innate immune defense machinery. Most importantly, multiple studies have reported dysregulation of lectins in neurological disorders. Here, we reviewed recent studies on microglial lectins and their functions in CNS health and disease, and suggest that these lectin families are novel, potent therapeutic targets for neurological diseases.

Dataset Information

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact.

Publications

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact.

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