2014
DOI: 10.1016/j.neurobiolaging.2013.11.006
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Age and duration of inflammatory environment differentially affect the neuroimmune response and catecholaminergic neurons in the midbrain and brainstem

Abstract: Neuroinflammation and degeneration of ascending catecholaminergic systems occur early in the neurodegenerative process. Age and the duration of a pro-inflammatory environment induced by continuous intraventricular lipopolysaccharide (LPS) differentially affect the expression profile of pro- and anti-inflammatory genes and proteins as well as the number of activated microglia (express major histocompatibility complex II, MHCII) and the integrity and density of ascending catecholaminergic neural systems originat… Show more

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Cited by 47 publications
(44 citation statements)
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“…Intranasal administration provides a non-invasive method which may bypass the blood-brain barrier (BBB) to deliver therapeutic agents to the central nervous system, and thus reducing systemic exposure and side effects [14, 15]. Studies by us and others have shown that IGF-1 can be delivered to the rodent brain along olfactory and trigeminal pathways with intranasal administration [14, 15], and that intranasally delivered IGF-1 protects against LPS-induced white matter injury in the developing rat brain [16], cerebral hypoxic-ischemic injury [1719], and other neurodegenerative damages [20, 21] which may be related to activation of intracellular signaling cascades such as the phophatidylinositol-3 kinase (PI3K)/Akt pathway [20, 23]. …”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Intranasal administration provides a non-invasive method which may bypass the blood-brain barrier (BBB) to deliver therapeutic agents to the central nervous system, and thus reducing systemic exposure and side effects [14, 15]. Studies by us and others have shown that IGF-1 can be delivered to the rodent brain along olfactory and trigeminal pathways with intranasal administration [14, 15], and that intranasally delivered IGF-1 protects against LPS-induced white matter injury in the developing rat brain [16], cerebral hypoxic-ischemic injury [1719], and other neurodegenerative damages [20, 21] which may be related to activation of intracellular signaling cascades such as the phophatidylinositol-3 kinase (PI3K)/Akt pathway [20, 23]. …”
Section: Introductionmentioning
confidence: 99%
“…The LPS-induced neuroinflammation and neurobehavioral dysfunction are involved not only in the substantia nigra (SN) [23, 24], but also in other central catecholaminergic neurons such as the dopaminergic neurons in the ventral tegmental area (VTA) of midbrain [23, 25] and olfactory bulb (OB) [26, 27], and the noradrenergic neurons in the locus coeruleus (LC) of the pons [23, 24]. The objective of the present study is to further examine whether IGF-1 delivered through intranasal route in the neonatal rat provides long-lasting protection against LPS-induced dopaminergic and noradrenergic neuronal injury, and ameliorates LPS-induced neurobehavioral dysfunction in juvenile rats.…”
Section: Introductionmentioning
confidence: 99%
“…Over the past decades, several mechanisms have been supposed to be involved in the pathogenesis of PD, including oxidative stress, mitochondrial dysfunction, protein misfolding and aggregation, apoptosis, and so on (Finsterer, 2011;Huang et al, 2012;Lee et al, 2015). In addition, many exciting discoveries have illustrated that chronic neuroninflammation characterized by the release of pro-inflammatory mediators from activated microglia also exerts an important effect on the pathophysiology of PD (Bardou et al, 2014;Borrajo et al, 2014). But how the inflammation is triggered in PD remains unclear.…”
Section: Introductionmentioning
confidence: 99%
“…Chronic neuroinflammation also appears early in the progression of AD and PD, with early stage AD and PD patients showing increased microglia activation in vulnerable brain regions (Yasuno et al, 2012; Iannaccone et al, 2013). The SNpc and LC are vulnerable to neuroinflammation (Bardou et al, 2014; Brothers et al, 2013). Major histocompatibility complex I (MHC-I) is expressed at very low levels in the CNS, although in the presence of neuroinflammation SN and LC neurons specifically upregulate MHC-I, which makes them selectively targeted for degradation (Cebrián et al, 2014).…”
Section: Introductionmentioning
confidence: 99%
“…Several aspects of early AD can be reproduced by chronic infusion of lipopolysaccharide (LPS) into the fourth ventricle of young rats (Hauss-Wegrzyniak et al, 1998a). This model may also be relevant for modeling early PD, since following chronic LPS administration in vivo , dopaminergic (DA) cell loss is observed in the SNpc and noradrenergic (NE) neuron loss is observed in the LC (Bardou et al, 2014). …”
Section: Introductionmentioning
confidence: 99%