Losing your nerves? Maybe it's the antibodies

Diamond, Betty; Huerta, Patricio T.; Mina‐Osorio, Paola; Kowal, Czeslawa; Volpe, Bruce T.

doi:10.1038/nri2529

Cited by 224 publications

(221 citation statements)

References 82 publications

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“…51 Here too, clinical studies aiming to correlate manifestations of neuropsychiatric SLE with NMDA receptor antibodies have yielded inconsistent results. 5 Future work will undoubtedly continue to examine whether the aforementioned antibodies and others are pathogenic in neuropsychiatric SLE.…”

Section: Encephalopathy In Lupus and Other Systemic Syndromesmentioning

confidence: 99%

“…1,4 Recently, a number of syndromes characterized in part by global encephalopathy or even more focal psychiatric changes have been found to result from autoimmune dysfunction, at times with autoantibodies that guide both diagnosis and treatment. 5,6 Here, we review autoimmune encephalitides caused by antineuronal antibodies that attack proteins involved in synaptic function, and we examine systemic autoimmune diseases that have profound neuropsychiatric components.…”

mentioning

confidence: 99%

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The Emerging Link Between Autoimmune Disorders and Neuropsychiatric Disease

Kayser¹,

Dalmau²

2011

Journal of Neuropsychiatry

115

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Section: Encephalopathy In Lupus and Other Systemic Syndromesmentioning

confidence: 99%

mentioning

confidence: 99%

The Emerging Link Between Autoimmune Disorders and Neuropsychiatric Disease

Kayser¹,

Dalmau²

2011

Journal of Neuropsychiatry

115

View full text Add to dashboard Cite

show abstract

“…Nicotine, stress, hypertensive episodes and inflammatory mediators secondary to infection and other insults have been demonstrated to increase permeability of the BBB (17)(18)(19), for which the former status as an impermeable barricade has evolved to that of a responsive gatekeeper with transport, secretory and signaling functions. Repeated episodes of increased BBB permeability over time may play a permissive role in allowing harmful molecules from the circulation access to the CNS, where they subsequently initiate neurotoxic events (20). We hypothesized that SLE patients with long-term (LT) disease duration would be more likely to have sustained repeated episodes of BBB disruption and would therefore display more neuronal dysfunction than patients with short-term (ST) disease duration.…”

Section: Differences In Regional Brain Activation Patterns Assessed Bmentioning

confidence: 99%

Differences in Regional Brain Activation Patterns Assessed by Functional Magnetic Resonance Imaging in Patients with Systemic Lupus Erythematosus Stratified by Disease Duration

Mackay

Bussa

Aranow

et al. 2011

Mol Med

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The mediators of tissue damage in systemic lupus erythematosus (SLE) such as antibodies, cytokines and activated immune cells have direct access to most organs in the body but must penetrate the blood-brain barrier (BBB) to gain access to brain tissue. We hypothesized that compromise of the BBB occurs episodically such that the brain will acquire tissue damage slowly and not at the same rate as other organs. On the basis of these assumptions, we wished to determine if duration of disease correlated with brain injury, as measured with functional magnetic resonance imaging (fMRI), and if this was independent of degree of tissue damage in other organs. We investigated differences in brain activation patterns using fMRI in 13 SLE patients stratified by disease duration of ≤2 years (short-term [ST]) or ≥10 years (long-term [LT]). Two fMRI paradigms were selected to measure working memory and emotional response (fearful faces task). Performance in the working memory task was significantly better in the ST group for one and two shape recall; however, both groups did poorly with three shape recall. Imaging studies demonstrated significantly increased cortical activation in the ST group in regions associated with cognition during the two shape retention phase of the working memory task (P < 0.001) and increased amygdala (P < 0.05) and superior parietal (P < 0.01) activation in response to the fearful faces paradigm. In conclusion, analysis of activation patterns stratified by performance accuracy, differences in comorbid disease, corticosteroid doses or disease activity suggests that these observed differences are attributable to SLE effects on the central nervous system exclusive of vascular disease or other confounding influences. Our hypothesis is further supported by the lack of correlation between regional brain abnormalities on fMRI and the Systemic Lupus International Collaborating Clinics (SLICC) damage index.

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“…The recently identified antibody against the potassium channel protein KIR4.1, for example, is detectable in not even 50% of MS patients [57]. In summary: No highly MS specific antigen or autoantibody signature could be identified yet [42,[58][59][60][61][62].…”

Section: Biomarker Candidates In the Central Nervous Systemmentioning

confidence: 99%

Molecular Biomarkers in Multiple Sclerosis

Paap

Hecker²,

Koczan³

et al. 2013

J Clin Cell Immunol

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Multiple Sclerosis (MS) is a chronic immune-modulated disorder of the central nervous system (CNS) affecting mainly young adults. Due to the complexity and heterogenic etiology of this disease diagnosis, treatment, and estimations concerning the future course of the disease for the individual patient are challenging. To encounter the variability in phenotype, disease progression and response to treatments, various new drugs are in development to complement existing treatment options. Since years intensive efforts are directed to identify biomarkers that are associated with various aspects of MS on different levels of the organizational hierarchy of the human body (e.g. DNA, RNA, proteins, cells).We researched the last ten years of literature to identify those proposed candidates that had been repeatedly published as being associated with MS etiology, clinical manifestation, disease course, and treatment response.Here, we present a categorized overview over molecular biomarkers in MS.However, despite of the large sum of studies and the long list of candidate markers, today only very few biomarkers are of clinical value. This is mostly due to lack of comparability and statistical power in most studies. However, there are recent advances in the field of applicable molecular biomarkers in MS: For example measurement of anti-AQP4 levels allows differentiation between neuromyelitis optica (NMO) and MS.

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Losing your nerves? Maybe it's the antibodies

Cited by 224 publications

References 82 publications

The Emerging Link Between Autoimmune Disorders and Neuropsychiatric Disease

The Emerging Link Between Autoimmune Disorders and Neuropsychiatric Disease

Differences in Regional Brain Activation Patterns Assessed by Functional Magnetic Resonance Imaging in Patients with Systemic Lupus Erythematosus Stratified by Disease Duration

Molecular Biomarkers in Multiple Sclerosis

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