Imaging multiple sclerosis and other neurodegenerative diseases

Inglese, Matilde; Petracca, Maria

doi:10.4161/pri.22650

Cited by 22 publications

(17 citation statements)

References 74 publications

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“…However, treating relapses with immunomodulatory therapies does not stop progression towards neurodegeneration and axonal loss, and as this effect indicates that the causes of lesions and neurodegeneration involve other mechanisms, key questions remain unanswered. Mechanisms underlying disease progression are proposed to involve an interaction between oxidative stress, mitochondrial dysfunction, energy deficit and ion channel dysfunction, which are also suggested to be involved in neurodegeneration in Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) 22 , 23 .…”

Section: Multiple Sclerosis As An Autoimmune Diseasementioning

confidence: 99%

Identification of brain antigens recognized by autoantibodies in experimental autoimmune encephalomyelitis-induced animals treated with etomoxir or interferon-β

Mørkholt

Kastaniegaard

Trabjerg

et al. 2018

Sci Rep

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Multiple sclerosis (MS) is a neurodegenerative autoimmune disease, where chronic inflammation plays an essential role in its pathology. A feature of MS is the production of autoantibodies stimulated by an altered-peptide-ligand response and epitope spreading, resulting in loss of tolerance for self-proteins. The involvement of autoantibodies in MS pathogenesis has been suggested to initiate and drive progression of inflammation; however, the etiology of MS remains unknown. The effect of etomoxir and interferon-β (IFN-β) was examined in an experimental-autoimmune-encephalomyelitis (EAE) model of MS. Moreover, the impact of etomoxir and IFN-β on recognition of brain proteins in serum from EAE rats was examined with the purpose of identifying the autoantibody reactivities involved in MS. Animals treated with etomoxir on day 1 exhibited a statistically significantly lower disease score than animals treated with IFN-β (on day 1 or 5) or placebo. Etomoxir treatment on day 5 resulted in a significantly lower disease score than IFN-β treatment on day 1. After disease induction antibodies was induced to a broad pallet of antigens in the brain. Surprisingly, by blocking CPT1 and therewith lipid metabolism several alterations in the antibody response was observed suggesting that autoantibodies play a role in the EAE animal model.

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Section: Multiple Sclerosis As An Autoimmune Diseasementioning

confidence: 99%

Identification of brain antigens recognized by autoantibodies in experimental autoimmune encephalomyelitis-induced animals treated with etomoxir or interferon-β

Mørkholt

Kastaniegaard

Trabjerg

et al. 2018

Sci Rep

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“…The very lively debate on the role of myeloid cells during neurodegeneration is caused by the uncertainties on their actual activation phenotype during disease development. This is due to the lack of handy investigation tools, such as appropriate biomarkers, to assess microglia activation in vivo , with the notable exception of PET imaging using the tracer [11C] (R)-PK11195 ( 9 ). The latter, however has low resolution and does not provide any information on the myeloid cell and activation phenotype.…”

Section: Myeloid Cells Phenotype In Admentioning

confidence: 99%

Myeloid Extracellular Vesicles: Messengers from the Demented Brain

et al. 2016

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Blood-borne monocyte derived cells play a pivotal, initially unrecognized, role in most central nervous system disorders, including diseases initially classified as purely neurodegenerative (i.e., Alzheimer’s disease, Parkinson’s disease, and ALS). Their trafficking to the brain and spinal cord has been extensively studied in classical neuroinflammatory disorders such as multiple sclerosis. Central nervous system resident myeloid cells, namely microglia and perivascular macrophages, also are in the spotlight of investigations on neurological disorders. Myeloid cells, such as infiltrating macrophages and microglia, have been described as having both protective and destructive features in neurological disorders, thus identification of their functional phenotype during disease evolution would be of paramount importance. Extracellular vesicles, namely exosomes and shed vesicles, are released by virtually any cell type and can be detected and identified in terms of cell origin in biological fluids. They therefore constitute an ideal tool to access information on cells residing in an inaccessible site such as the brain. We will review here available information on extracellular vesicles detection in neurological disorders with special emphasis on neurodegenerative diseases.

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“…Neurodegenerative diseases are known to be related to oxidative stress which is due to an imbalance between the production of reactive oxygen species (ROS) and the ability of intrinsic antioxidant systems, both enzymatic and non-enzymatic, to scavenge these radicals [1]. Oxidation of macromolecules such as proteins, lipids and DNA may lead to cell degeneration and death due to an increase in the release of apoptotic-inducing factors.…”

Section: Abstract Antioxidant • Neuroprotection • Anthocyanidins • Cmentioning

confidence: 99%

Protective Effect of Anthocyanidins on Astrocytes and Apoptosis Induced by Oxidative Damage

et al. 2015

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!As a result of the longer life expectancy in the human population, neurodegenerative diseases are increasing, so finding effective treatments together with prevention strategies are urgently needed. Anthocyanins are polyphenolic compounds from vegetal species that have shown strong antioxidant and anti-inflammatory activities in various experimental models. The effect of the anthocyanidins cyanidin, malvidin, and pelargonidin at different concentrations (5 to 100 µM) on experimental models of cell oxidation and apoptosis was studied and compared with the positive control Trolox. The human astrocyte glioblastoma, cellular line U373, was used for a cellular injury model using Fentonʼs reagent (0.5 mM FeSO 4 /1 mM H 2 O 2 ) and to measure the lactate dehydrogenase enzyme activities and lipid peroxidation level (thiobarbituric acid reactive substances) by fluorimetric analysis and malondialdehyde release by HPLC. Also, caspase 3, 8, and 9 activities were measured by fluorimetric analysis. The results show that the studied anthocyanidins are able to revert the induced apoptosis related to caspase activation and lipid peroxidation. All the assayed anthocyanidins significantly decreased the activation of caspases 8 and 3, although malvidin and cyanidin increased the activity of caspase 9 when compared to non-treated cells.Key words antioxidant · neuroprotection · anthocyanidins · cyanidin · pelargonidin · malvidin · oxidative stress Neurodegenerative diseases are known to be related to oxidative stress which is due to an imbalance between the production of reactive oxygen species (ROS) and the ability of intrinsic antioxidant systems, both enzymatic and non-enzymatic, to scavenge these radicals [1]. Oxidation of macromolecules such as proteins, lipids and DNA may lead to cell degeneration and death due to an increase in the release of apoptotic-inducing factors. Thus, different strategies have been proposed for the prevention and treatment of ROS-mediated diseases, with special emphasis on antioxidant therapy [2][3][4]. Anthocyanidins are polyphenols with a strong scavenging activity, which is related to their phenolic structure characterized by B ring hydroxyl groups and a conjugated double bond system. Orally administered anthocyanins have been proven to suppress stress-induced cerebral oxidative damage [5], reduce lipid peroxidation, increase glutathione levels and antioxidant enzymes activity, and improve spatial memory in the hippocampus of the adult rat [6]. In this study, we analyzed the antioxidant activity of the anthocyanidins cyanidin, malvidin, and pelargonidin at different concentrations on the human astrocyte glioblastoma, which is known as a useful model for the study of astrocyte functions under both physiological and pathological conditions. Then, the potential protective effect of these compounds against an oxidative injury chemically induced by Fentonʼs reagent, which induces a double-strand DNA breaking, was assessed [7]. For this purpose, lactate dehydrogenase (LDH) activity and the lipid...

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Imaging multiple sclerosis and other neurodegenerative diseases

Cited by 22 publications

References 74 publications

Identification of brain antigens recognized by autoantibodies in experimental autoimmune encephalomyelitis-induced animals treated with etomoxir or interferon-β

Identification of brain antigens recognized by autoantibodies in experimental autoimmune encephalomyelitis-induced animals treated with etomoxir or interferon-β

Myeloid Extracellular Vesicles: Messengers from the Demented Brain

Protective Effect of Anthocyanidins on Astrocytes and Apoptosis Induced by Oxidative Damage

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