Neuregulin-1: A Potential Endogenous Protector in Perinatal Brain White Matter Damage

Dammann, Olaf; Bueter, Wolfgang; Leviton, Alan; Gressèns, Pierre; Dammann, Christiane E.L.

doi:10.1159/000111119

Cited by 29 publications

(24 citation statements)

References 174 publications

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“…The association of later adverse outcomes with the presence of early-life circulating inflammatory proteins probably is modulated by other factors associated with immaturity, including the availability of endogenous protective factors (72),(73),(74) , such as oligotrophins. Heightened production and availability of oligotrophins could modulate the damaging effects associated with inflammation, for example, by enhancing cell development and/or survival (73) .…”

Section: Discussionmentioning

confidence: 99%

Circulating Inflammatory-Associated Proteins in the First Month of Life and Cognitive Impairment at Age 10 Years in Children Born Extremely Preterm

Kuban

Joseph

O’Shea

et al. 2017

The Journal of Pediatrics

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Objectives To evaluate whether in children born extremely preterm, indicators of sustained systemic inflammation in the first month of life are associated with cognitive impairment at school age. Study design 873 of 966 eligible children previously enrolled in the multicenter Extremely Low Gestational Age Newborn Study from 2002–2004 were evaluated at age 10 years. We analyzed the relationship between elevated blood concentrations of inflammation-associated proteins in the first 2 weeks (“early elevations”; n=812) and the 3rd and 4th week (“late elevations”; n=532) of life with neurocognition. Results Early elevations of CRP, TNF-alpha, IL-8, ICAM-1, and EPO were associated with IQ values >2 SD below the expected mean (ORs: 2.0–2.3) and with moderate to severe cognitive impairment on a composite measure of IQ and executive function (ORs: 2.1–3.6). Additionally, severe cognitive impairment was associated with late protein elevations of CRP (OR:4.0; 95% CI 1.5, 10), IL-8 (OR:5.0; 1.9, 13), ICAM-1 (OR:6.5; 2.6, 16), VEGF-R2 (OR:3.2; 1.2, 8.3), and TSH (OR:3.1; 1.3, 7.3). Moderate cognitive impairment was most strongly associated with elevations of IL-8, ICAM-1, and VEGF-R2. When four or more inflammatory proteins were elevated early, the risk of having an IQ<70 and having overall impaired cognitive ability was more than doubled (ORs:2.1–2.4); the presence of four or more inflammatory protein elevated late was strongly linked to adverse cognitive outcomes (ORs:2.9–4.8). Conclusion EP children who had sustained elevations of inflammation-related proteins in the first postnatal month are more likely than EP peers without such elevations to have cognitive impairment at 10 years.

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Section: Discussionmentioning

confidence: 99%

Circulating Inflammatory-Associated Proteins in the First Month of Life and Cognitive Impairment at Age 10 Years in Children Born Extremely Preterm

Kuban

Joseph

O’Shea

et al. 2017

The Journal of Pediatrics

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“…Cognitive and neurological impairments have been observed after in-utero exposure to infection and appear to correlate with changes in white matter around the ventricles, termed periventricular leukomalacia (Dammann and Leviton, 1997;Favrais et al, 2011;Sorensen et al, 2006;Chew et al, 2013;Hagberg et al, 2012). The subsequent pro-inflammatory changes and microglial activation in periventricular leukomalacia seem to act as mediators of CNS inflammation (Dammann et al, 2008;Leviton and Gressens, 2007). During the developmental insult, cytokines such as IL-8 (Brown et al, 2004) and TNF-alpha (Buka et al, 2001b) appear to circulate at higher blood levels in the maternal blood of individuals later at risk for psychotic disorders.…”

Section: Systemic Infections and Neurodevelopmental Mechanismsmentioning

confidence: 99%

Clinical studies of neuroinflammatory mechanisms in schizophrenia

Watkins

Andrews

2016

Schizophrenia Research

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“…Neuregulin-1 (NRG1), a growth factor with multiple isoforms acting on different pathways, has been reported to have possible neuroprotective effects in CNS injury (Dammann et al, 2008; Li et al, 2007; Shyu et al, 2004). In a rat model of stroke with MCAO, immunohistochemical staining 3 days after injury revealed an increase in NRG-1 expression in the penumbral regions of the cortex (Parker et al, 2002).…”

Section: Factors Affecting Remyelination After Strokementioning

confidence: 99%

Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

et al. 2015

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White matter damage is a clinically important aspect of several central nervous system diseases, including stroke. Cerebral white matter primarily consists of axonal bundles ensheathed with myelin secreted by mature oligodendrocytes, which play an important role in neurotransmission between different areas of gray matter. During the acute phase of stroke, damage to oligodendrocytes leads to white matter dysfunction through the loss of myelin. On the contrary, during the chronic phase, white matter components promote an environment, which is favorable for neural repair, vascular remodeling, and remyelination. For effective remyelination to take place, oligodendrocyte precursor cells (OPCs) play critical roles by proliferating and differentiating into mature oligodendrocytes, which help to decrease the burden of axonal injury. Notably, other types of cells contribute to these OPC responses under the ischemic conditions. This mini-review summarizes the non-cell autonomous mechanisms in oligodendrogenesis and remyelination after white matter damage, focusing on how OPCs receive support from their neighboring cells.

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Neuregulin-1: A Potential Endogenous Protector in Perinatal Brain White Matter Damage

Cited by 29 publications

References 174 publications

Circulating Inflammatory-Associated Proteins in the First Month of Life and Cognitive Impairment at Age 10 Years in Children Born Extremely Preterm

Circulating Inflammatory-Associated Proteins in the First Month of Life and Cognitive Impairment at Age 10 Years in Children Born Extremely Preterm

Clinical studies of neuroinflammatory mechanisms in schizophrenia

Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

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