The Role of Immune and Inflammatory Mechanisms in ALS

McCombe, P. A.; Henderson, R D.

doi:10.2174/1566211213754895240

Cited by 27 publications

(27 citation statements)

References 101 publications

(115 reference statements)

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“…Single nucleotide polymorphism rs4074082 is close to the complement C1q tumor necrosis factor‐related protein‐7 gene, which plays a role in neural inflammation (Figure B). The expression of complement C1q tumor necrosis factor‐related protein‐7 was found to be downregulated in amyotrophic lateral sclerosis, a neurodegenerative disorder in which abnormal inflammatory response is involved as part of the etiology . rs9772881 is approximate to the TSNARE1 gene locus.…”

Section: Genetic Determinants Of Subgingival Bacterial Colonizationmentioning

confidence: 99%

Periodontal inflammation: Integrating genes and dysbiosis

Zhang

Yu²,

Arce

2019

Periodontology 2000

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Biofilm bacteria co‐evolve and reach a symbiosis with the host on the gingival surface. The disruption of the homeostatic relationship between plaque bacteria and the host can initiate and promote periodontal disease progression. Recent advances in sequencing technologies allow researchers to profile disease‐associated microbial communities and quantify microbial metabolic activities and host transcriptional responses. In addition to confirming the findings from previous studies, new putative pathogens and novel genes that have not previously been associated with periodontitis, emerge. For example, multiple studies have reported that Synergistetes bacteria are associated with periodontitis. Genes involved in epithelial barrier defense were downregulated in periodontitis, while excessive expression of interleukin‐17 was associated with a hyperinflammatory response in periodontitis and with a unique microbial community. Bioinformatics‐enabled gene ontology pathway analyses provide a panoramic view of the bacterial and host activities as they shift from periodontal health to disease. Additionally, host innate factors, such as genetic variants identified by either a candidate‐gene approach or genome‐wide association analyses, have an impact on subgingival bacterial colonization. Transgenic mice carrying candidate genetic variants, or with the deletion of candidate genes mimicking the deleterious loss‐of‐function variant effect, provide experimental evidence validating the biologic relevance of the novel markers associated with the microbial phenotype identified through a statistical approach. Further refinement in bioinformatics, data management approaches, or statistical tools, are required to gain insight into host‐microbe interactions by harmonizing the multidimensional “big” data at the genomic, transcriptional, and proteomic levels.

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Section: Genetic Determinants Of Subgingival Bacterial Colonizationmentioning

confidence: 99%

Periodontal inflammation: Integrating genes and dysbiosis

Zhang

Yu²,

Arce

2019

Periodontology 2000

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“…It has been reported by AL-Chalabi et al that ALS appears to have a lot of similarity with cancer and that it occurs with the effect of multistage environmental factors as time progresses in genetically susceptible individuals [32 and 33]. How inflammation contributes to pathogenesis of various neurodegenerative diseases, including ALS [34], Alzheimer's disease (AD) [34 and 35], and Parkinson's disease (PD) [36] is still unclear and involves a very complex process. Inflammatory processes have been discussed in neuropathological studies on motor system of ALS patients [34, 37 and 38].…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid (Csf) Il-17a, Il-17f, Il-34 and CXCL-13 Levels in Amyotrophic Lateral Sclerosis (Als/Mnd) Patients

Orallar¹,

Karaböcek²,

Bozat³

et al. 2019

NWSA

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In this study, our clinic follow-up ALS/MND diagnose the cerebrospinal fluid of patients (CSF), IL-17A, IL-17F, IL-34 cytokines and CXCL-13 chemokine to evaluate the levels. that were determined by ELISA. In our study, significantly higher in the patient group and the proinflammatory cytokine, IL-17A and IL-17F of endothelial cells, fibroblasts and also known to be expressed in neurones. However, CXCL-13 level is considered among the patient group and the control group was not statistically significant difference. IL-34 also to be increased when compared to the patient group (n=4) than the control group (n=6), a recently described cytokine due to the IL-34 Th17 with modulating immune pathogenesis and immune with cytokines released from cells in a short time to be involved ALS/MND such as rare as to be made further studies for the diagnosis of a disease to a powerful new biomarker may and science has been suggested to contribute in this respect.

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“…Amyotrophic lateral sclerosis (ALS) is a progressive disease caused by neuroinflammation, primarily in motor neurons, resulting in muscle weakness and loss of voluntary muscle control . Several genetic mutations ( ALS2 , FUS , and SOD1 ) have been attributed as an etiology or risk factor for ALS…”

Section: Kidney Disease and Transporters Final Remarksmentioning

confidence: 99%

Effect of Disease Pathologies on Transporter Expression and Function

Atilano-Roque

Roda

Fogueri

et al. 2016

The Journal of Clinical Pharma

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Transporters are important determinants of drug absorption, distribution, and excretion. The clinical relevance of drug transporters in drug disposition and toxicology depends on their localization in liver, kidney, and brain. There has been growing evidence regarding the importance of disease status on alterations in metabolizing enzymes and transporter proteins. This review focuses on uptake and efflux transporter proteins in liver, kidney, and brain and discusses mechanisms of altered transporter expression and function secondary to disease.

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The Role of Immune and Inflammatory Mechanisms in ALS

Cited by 27 publications

References 101 publications

Periodontal inflammation: Integrating genes and dysbiosis

Periodontal inflammation: Integrating genes and dysbiosis

Cerebrospinal Fluid (Csf) Il-17a, Il-17f, Il-34 and CXCL-13 Levels in Amyotrophic Lateral Sclerosis (Als/Mnd) Patients

Effect of Disease Pathologies on Transporter Expression and Function

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