Distribution of Iron, Copper, Zinc and Cadmium in Glia, Their Influence on Glial Cells and Relationship with Neurodegenerative Diseases
Aleksandra GórskaAgnieszka Markiewicz-GospodarekRenata MarkiewiczZuzanna ChilimoniukBartosz BorowskiMateusz TrubalskiKatarzyna Czarnek
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Recent data on the distribution and influence of copper, zinc and cadmium in glial cells are summarized. This review also examines the relationship between those metals and their role in neurodegenerative diseases like Alzheimer disease, multiple sclerosis, Parkinson disease and Amyotrophic lateral sclerosis, which have become a great challenge for today’s physicians. The studies suggest that among glial cells, iron has the highest concentration in oligodendrocytes, copper in astrocytes and zinc in the glia of hippocampus and cortex. Previous studies have shown neurotoxic effects of copper, iron and manganese, while zinc can have a bidirectional effect, i.e., neurotoxic but also neuroprotective effects depending on the dose and disease state. Recent data point to the association of metals with neurodegeneration through their role in the modulation of protein aggregation. Metals can accumulate in the brain with aging and may be associated with age-related diseases.Keywords:
Neurotoxicity
Neuroglia
ALS : amyotrophic lateral sclerosis UMN : upper motor neuron LMN : lower motor neuron fALS : familial amyotrophic lateral sclerosis sALS : sporadic amyotrophic lateral sclerosis Amyotrophic lateral sclerosis (ALS) reflects a heterogeneous group of neurodegenerative disorders unified by
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Sera from patients with amyotrophic lateral sclerosis (ALS) were applied to mouse anterior horn cells in tissue culture. No unique toxic effect was observed when compared with sera from normal and non-ALS neuromuscular disease subjects.
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Amyotrophic lateral sclerosis is a rarely seen degenerative disease which involves the upper and lower motor neuron.In the past few years,significant progresses have been made in this disease.The article reviews the current diagnosis and treatment of amyotrophic lateral sclerosis.
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Our modern era is witnessing an increased prevalence of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and brain tumors. This is accompanied by an increased production of nanoparticles (NPs) and the subsequent release of NPs in the environment shared by humans. NPs are extremely small molecules measuring about 100 nm in diameter. Due to minuscule size, NPs have the potential to penetrate human body through various pathways and eventually cross the blood-brain barrier to potentially cause neurotoxicity, neuroinflammation and neurodegeneration of the central nervous system. Until recently, the mechanisms by which NPs cause neuroinflammation and neurodegeneration were unknown. However, recent in vivo, ex vivo and in vitro studies have significantly advanced our understanding of the mechanisms by which NPs may cause neurotoxicity and neurodegeneration. In light of this understanding, various pathways have been identified as the basic mechanisms by which NPs cause damage in the brain. The goal of this review is to summarize new mechanistic findings and different pathways of NP-induced neurotoxicity. Better knowledge of such pathways can lead researchers to devise effective therapeutic strategies for neuroprotection against nanoparticles. Keywords: Alzheimer's disease, microglia activation, nanoparticles, neurodegenerative, oxidative stress, Parkinson's disease.
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AMA Pluta R, Bogucka-Kocka A, Ułamek-Kozioł M, et al. Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica. 2015;53(2):89-99. doi:10.5114/fn.2015.52405. APA Pluta, R., Bogucka-Kocka, A., Ułamek-Kozioł, M., Furmaga-Jabłońska, W., Januszewski, S., & Brzozowska, J. et al. (2015). Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica, 53(2), 89-99. https://doi.org/10.5114/fn.2015.52405 Chicago Pluta, Ryszard, Anna Bogucka-Kocka, Marzena Ułamek-Kozioł, Wanda Furmaga-Jabłońska, Sławomir Januszewski, Judyta Brzozowska, and Mirosław Jabłoński et al. 2015. "Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?". Folia Neuropathologica 53 (2): 89-99. doi:10.5114/fn.2015.52405. Harvard Pluta, R., Bogucka-Kocka, A., Ułamek-Kozioł, M., Furmaga-Jabłońska, W., Januszewski, S., Brzozowska, J., Jabłoński, M., and Kocki, J. (2015). Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica, 53(2), pp.89-99. https://doi.org/10.5114/fn.2015.52405 MLA Pluta, Ryszard et al. "Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?." Folia Neuropathologica, vol. 53, no. 2, 2015, pp. 89-99. doi:10.5114/fn.2015.52405. Vancouver Pluta R, Bogucka-Kocka A, Ułamek-Kozioł M, Furmaga-Jabłońska W, Januszewski S, Brzozowska J et al. Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica. 2015;53(2):89-99. doi:10.5114/fn.2015.52405.
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Abstract Phosphorylated TDP-43 (pTDP-43) aggregates in the cytoplasm of motor neurons and neuroglia in the brain are one of the pathological hallmarks of amyotrophic lateral sclerosis. Although the axons exceed the total volume of motor neuron soma by several orders of magnitude, systematic studies investigating the presence and distribution of pTDP-43 aggregates within motor nerves are still lacking. The aim of this study is to define the TDP-43/pTDP-43 pathology in diagnostic motor nerve biopsies performed on a large cohort of patients presenting with a lower motor neuron syndrome and to assess whether this might be a discriminating tissue biomarker for amyotrophic lateral sclerosis and non-amyotrophic lateral sclerosis cases. We retrospectively evaluated 102 lower motor neuron syndrome patients referred to our centre for a diagnostic motor nerve biopsy. Histopathological criteria of motor neuron disease and motor neuropathy were applied by two independent evaluators, who were blind to clinical data. TDP-43 and pTDP-43 were evaluated by immunohistochemistry, and results compared to final clinical diagnosis. We detected significant differences between amyotrophic lateral sclerosis and non-amyotrophic lateral sclerosis cases in pTDP-43 expression in myelinated fibres: axonal accumulation was detected in 98.2% of patients with amyotrophic lateral sclerosis versus 30.4% of non-amyotrophic lateral sclerosis samples (P < 0.0001), while concomitant positive staining in Schwan cell cytoplasm was found in 70.2% of patients with amyotrophic lateral sclerosis versus 17.4% of patients who did not have amyotrophic lateral sclerosis (P < 0.001). Importantly, we were also able to detect pTDP-43 aggregates in amyotrophic lateral sclerosis cases displaying normal features at standard histopathological analysis. Our findings demonstrated that a specific pTDP-43 signature is present in the peripheral nervous system of patients with amyotrophic lateral sclerosis, and could be exploited as a specific, accessible tissue biomarker. The detection of pTDP-43 aggregates within motor nerves of living patients with amyotrophic lateral sclerosis, occurring before axonal degeneration, suggests that this is an early event that may contribute to amyotrophic lateral sclerosis pathogenesis.
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