Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D deficiency is associated with a higher risk of multiple sclerosis and also with a higher relapse rate as well as a higher number of MRI lesions. Elders with vitamin D deficiency have worse cognitive performance. Vitamin D deficiency is a risk factor for developing Alzheimer's disease. Ischemic stroke are more frequent and more severe in patients with low vitamin D levels. Carotid atherosclerosis is more frequent and more severe in patients with vitamin D deficiency. Vitamin D deficiency is associated with a higher risk and worse prognosis of Parkinson's disease. In the different neurological disorders discussed herein, gene polymorphisms that could alter vitamin D metabolism are also associated with a higher incidence or a worse disease prognosis. Despite the links between vitamin D deficiency and the risks of developing neurological disorders, there is, to date, no proof that supplementation could alter the course of these diseases.
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PMID:[Vitamin D and neurology]. 2405 66

As the first line of defense in the nervous system, resident microglia are the predominant immune cells in the brain. In diseases of the central nervous system such as stroke, Alzheimer's disease, and Parkinson's disease, they often cause inflammation or phagocytosis; however, some studies have found that despite the current controversy over M1, M2 polarization could be beneficial. Ischemic stroke is the third most common cause of death in humans. Patients who survive an ischemic stroke might experience a clear decline in their quality of life, owing to conditions such as hemiplegic paralysis and aphasia. After stroke, the activated microglia become a double-edged sword, with distinct phenotypic changes to the deleterious M1 and neuroprotective M2 types. Therefore, methods for promoting the differentiation of microglia into the M2 polarized form to alleviate harmful reactions after stroke have become a topic of interest in recent years. Subsequently, the discovery of new drugs related to M2 polarization has enabled the realization of targeted therapies. In the present review, we discussed the neuroprotective effects of microglia M2 polarization and the potential mechanisms and drugs by which microglia can be transformed into the M2 polarized type after stroke.
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PMID:Treatment targets for M2 microglia polarization in ischemic stroke. 2988 47

Ischemic stroke is responsible for a large number of neurological deficits including memory impairment. Deep brain stimulation (DBS), a well established therapeutic modality for the treatment of movement disorders, has recently shown potential beneficial effects on memory in animals and patients with Alzheimer's disease. Here, we test DBS for its ability to improve memory impairments by stimulating the entorhinal cortex (EC) in a rat model of global ischemia (GI). Two weeks after GI, adult male rats received high-frequency EC DBS for 1 h, and animals were assessed for changes in locomotor activity, learning, and memory 6 weeks later. GI produced spatial memory impairment that was ameliorated by DBS, with no difference between the group that received DBS for GI (GI-DBS ON group) and nonstroke control groups. Although GI led to a dramatic CA1 neuronal loss that could not be rescued with DBS, stimulation attenuated the reduction of CA1 synaptophysin expression after GI. Further, in vitro slice recordings showed a restoration of typical evoked synaptic dendritic fields in GI-DBS ON animals, indicating that the DBS-induced memory rescue is associated with increased synaptophysin expression and enhanced synaptic function. These results suggest that DBS may ameliorate the functional consequences of cerebral ischemia and point to be a potential new therapeutic approach.SIGNIFICANCE STATEMENT Deep brain stimulation (DBS) is remarkably effective in treating Parkinson's disease and is currently under investigation for the treatment of neuropsychiatric disorders including Alzheimer's disease. Until now, DBS has not been examined for its cognitive benefits in the context of hypoxic-ischemic injuries. Here, we investigated the effect of DBS in a rat model of global ischemia (GI) that mimics the neurological consequences occurring after a cardiac arrest. We show that DBS rescues memory deficits induced by GI and produces changes in synaptic activity in the hippocampus. Novel approaches to improve neurological outcomes after stroke are urgently needed; therefore, the present study highlights a possible role for DBS in the treatment of cognitive impairment associated with ischemia.
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PMID:Deep Brain Stimulation Rescues Memory and Synaptic Activity in a Rat Model of Global Ischemia. 3069 31

Ischemic stroke (IS) and Parkinson's disease (PD) are two neurological diseases that often strike individuals of advanced age. Although thought of as a disease of old age, PD can occur in younger patients. In many of these cases, genetic mutations underlie the disease. As with PD, stroke can also have a genetic component. Although many of the risk factors for IS are considered to be modifiable, a significant portion is not, suggesting that some of stroke risk factors may have a genetic origin. Large-scale genome-wide association studies (GWAS) have identified several IS and PD gene variants recently. Converging epidemiologic and pathological evidence suggests that IS and PD may be linked. However, it is still unclear whether these two conditions share a common mechanism. Here, we sought to determine the genetic mechanism underlying the possible association between IS and PD. We conducted a multi-step systemic analysis comprising (1) identification of IS and PD variants validated by known GWAS, (2) two separate gene-based tests using Versatile Gene-based Association Study 2 (VEGAS2) and PLINK, (3) a transcriptome-wide association study (TWAS), and (4) analyses of gene expression using an online tool in Gene Expression Omnibus. Our investigation revealed that IS and PD have in common five shared genes: GPX7, LBH, ZCCHC10, DENND2A, and NUDT14, which pass gene-based tests. Functionally, these genes are expressed differentially in IS and PD patients compared to neurologically healthy control subjects. This genetic overlap may provide clues on how IS and PD are linked mechanistically. This new genetic insight into these two diseases may be very valuable for narrowing the focus of future studies on the genetic basis of IS and PD and for developing novel therapies.
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PMID:Identification of Shared Genes Between Ischemic Stroke and Parkinson's Disease Using Genome-Wide Association Studies. 3098 2