Role of Scavenger Receptors in Glia-Mediated Neuroinflammatory Response Associated with Alzheimer’s Disease

Cornejo, Francisca; Bernhardi, Rommy von

doi:10.1155/2013/895651

Cited by 26 publications

(22 citation statements)

References 131 publications

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“…Similar observations have been made in animal models of AD , although evidence of microglial activation and astroglial activation is not confined to areas of plaque deposition but widespread throughout the brain Kelly et al 2013). The combination of activated glia (Cornejo and von Bernhardi 2013) and infiltrating T cells (Hartwig 1995;McGeer et al 1989;Parachikova et al 2007;Pirttila et al 1992;Rogers et al 1988;Togo et al 2002; in AD raises the possibility that these APCs can interact with T cells and potentially exacerbate the existing inflammation. The ability of microglia to act as APCs is examined more frequently in the context of MS and EAE; here increased expression of MHC class II, CD80 and CD40 on microglia (Chastain et al 2011;Murphy et al 2010) coincides with the large numbers of auto-reactive T cells that enter the brain and play a central role in disease pathogenesis (Fletcher et al 2010).…”

Section: Microglia As Apcssupporting

confidence: 63%

T Cells—Protective or Pathogenic in Alzheimer’s Disease?

McManus

Mills

Lynch

2015

J Neuroimmune Pharmacol

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Alzheimer's disease (AD) is the most common cause of dementia, and is characterised by deposits of amyloid β (Aβ), neurofibrillary tangles and neuronal loss. Neuroinflammatory changes have been identified as a feature of the disease, and recent studies have suggested a potential role for the peripheral immune system in driving these changes and, ultimately, the associated neuronal degeneration. A number of reports have detailed changes in the activation state and subtype of T cells in the circulation and CSF of AD patients and there is evidence of T cell infiltration into the brain. In this review, we examine the possible impact of T cell infiltration in the progression of pathology in AD and consider the data obtained from animal models of the disease. We consider how these cells infiltrate the brain, particularly in AD, and discuss whether the presence of T cells in the AD brain is protective or pathogenic. Finally we evaluate the current therapies, particularly those that involve immunization.

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Section: Microglia As Apcssupporting

confidence: 63%

T Cells—Protective or Pathogenic in Alzheimer’s Disease?

McManus

Mills

Lynch

2015

J Neuroimmune Pharmacol

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“…On the other hand, activated microglia found in the periphery of Aβ plaques could also release pro-inflammatory cytokines, thereby increasing oxidative stress. 100,101 Astrocytic Aβ peptide Accumulating data show the importance of astrocytes in Aβ pathogenesis in AD. Numerous debates have discussed whether astrocytes uptake Aβ from the extracellular space or they could synthesize Aβ de novo.…”

Section: Other Glial Cells In Ischemiamentioning

confidence: 99%

The neglected co-star in the dementia drama: the putative roles of astrocytes in the pathogeneses of major neurocognitive disorders

Law

Chung

2014

Mol Psychiatry

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Alzheimer's disease (AD) and vascular dementia are the major causes of cognitive disorders worldwide. They are characterized by cognitive impairments along with neuropsychiatric symptoms, and that their pathogeneses show overlapping multifactorial mechanisms. Although AD has long been considered the most common cause of dementia, individuals afflicted with AD commonly exhibit cerebral vascular abnormalities. The concept of mixed dementia has emerged to more clearly identify patients with neurodegenerative phenomena exhibiting both AD and cerebral vascular pathologies-vascular damage along with β-amyloid (Aβ)-associated neurotoxicity and τ-hyperphosphorylation. Cognitive impairment has long been commonly explained through a 'neuro-centric' perspective, but emerging evidence has shed light over the important roles that neurovascular unit dysfunction could have in neuronal death. Moreover, accumulating data have been demonstrating astrocytes being the essential cell type in maintaining proper central nervous system functioning. In relation to dementia, the roles of astrocytes in Aβ deposition and clearance are unclear. This article emphasizes the multiple events triggered by ischemia and the cytotoxicity exerted by Aβ either alone or in association with endothelin-1 and receptor for advanced glycation end products, thereby leading to neurodegeneration in an 'astroglio-centric' perspective.

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“…On the other hand, phagocytosis under pathological conditions has been related to a bouquet of molecules and pathways including pattern recognition receptors such as the receptor for advanced glycation endproducts (RAGE) and Toll‐like receptors (TLRs) and scavenger receptors (Loov et al . ; Cornejo and von Bernhardi ; Villarreal et al . ; Ponath et al .…”

Section: Discussionmentioning

confidence: 99%

G5G2.5 core‐shell tecto‐dendrimer specifically targets reactive glia in brain ischemia

Murta

Schilrreff

Rosciszewski

et al. 2018

Journal of Neurochemistry

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Secondary neuronal death is a serious stroke complication. This process is facilitated by the conversion of glial cells to the reactive pro-inflammatory phenotype that induces neurodegeneration. Therefore, regulation of glial activation is a compelling strategy to reduce brain damage after stroke. However, drugs have difficulties to access the CNS, and to specifically target glial cells. In the present work, we explored the use core-shell polyamidoamine tecto-dendrimer (G5G2.5 PAMAM) and studied its ability to target distinct populations of stroke-activated glial cells. We found that G5G2.5 tecto-dendrimer is actively engulfed by primary glial cells in a time- and dose-dependent manner showing high cellular selectivity and lysosomal localization. In addition, oxygen-glucose deprivation or lipopolysaccharides exposure in vitro and brain ischemia in vivo increase glial G5G2.5 uptake; not being incorporated by neurons or other cell types. We conclude that G5G2.5 tecto-dendrimer is a highly suitable carrier for targeted drug delivery to reactive glial cells in vitro and in vivo after brain ischemia.

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Role of Scavenger Receptors in Glia-Mediated Neuroinflammatory Response Associated with Alzheimer’s Disease

Cited by 26 publications

References 131 publications

T Cells—Protective or Pathogenic in Alzheimer’s Disease?

T Cells—Protective or Pathogenic in Alzheimer’s Disease?

The neglected co-star in the dementia drama: the putative roles of astrocytes in the pathogeneses of major neurocognitive disorders

G5G2.5 core‐shell tecto‐dendrimer specifically targets reactive glia in brain ischemia

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