The role of soluble intercellular adhesion molecules in neurodegenerative disorders

Rentzos, Michael; Michalopoulou, Maria; Nikolaou, Chryssoula; Cambouri, C.; Rombos, A.; Dimitrakopoulos, Antonios; Vassilopoulos, Demetrios

doi:10.1016/j.jns.2004.11.001

Cited by 45 publications

(32 citation statements)

References 56 publications

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“…Our current and previous data suggest that systemic inflammation, and the related increase of sEselectin plasma levels, might play a role in cerebrovascular disease. On the other hand, our results confirm the findings of Rentzos et al [37] who found similar levels of sE-selectin in plasma of patients with LOAD and in controls [37].…”

Section: Soluble E-selectin (Se-selectin)supporting

confidence: 93%

Markers of endothelial dysfunction in older subjects with late onset Alzheimer's disease or vascular dementia

Zuliani

Cavalieri

Galvani

et al. 2008

Journal of the Neurological Sciences

150

114

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Section: Soluble E-selectin (Se-selectin)supporting

confidence: 93%

Markers of endothelial dysfunction in older subjects with late onset Alzheimer's disease or vascular dementia

Zuliani

Cavalieri

Galvani

et al. 2008

Journal of the Neurological Sciences

150

114

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“…Our data extend previous findings showing that intracellular adhesion molecules extracted by blood monocytes in AD patients were reduced (Hochstrasser et al 2010). On the other hand increase soluble PECAM and ICAM from AD plasma (Nielsen et al 2007;Rentzos et al 2005) and ICAM-1 accumulated in brain senile plaques of AD were observed (Eikelenboom et al 1994).…”

Section: Discussionmentioning

confidence: 96%

Reduced plasma levels of P-selectin and L-selectin in a pilot study from Alzheimer disease: relationship with neuro-degeneration

et al. 2011

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Neurodegenerative processes associated with Alzheimer's disease (AD) are accompanied by reactive astrogliosis and microglia activation and a role for chronic inflammation in the brain degeneration of these patients has been suggested. Moreover impaired immune functions in AD brains might also influence the disease's progression. Therefore, it is of interest to further characterized inflammatory molecules in the peripheral blood of patients with AD and its relationship with cognitive decline. A complex picture emerged in this pilot study and IL-8, IFN-gamma, MCP-1 and VEGF levels were increased in AD. Levels of P-selectin and L-selectin were decreased in AD and lowest in AD patients with highest cognitive decline. Our findings suggest that these molecules may induce alterations of endothelial regulation and influence neurodegenerative processes of AD.

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“…The above reported observations show a link between ICAM-1 expression and AD, both in vivo and in vitro. Interestingly, the increased expression of ICAM-1 is not lim-ited to the brain, but it has also been shown in the periphery of AD patients [30,31]. More recently, soluble ICAM-1 was identified as one of the specific markers of AD and as a predictor of progression from mild cognitive impairment, the pre-clinical form of the disease, to AD [32].…”

Section: Discussionmentioning

confidence: 99%

Increased Pro-Inflammatory Response by Dendritic Cells from Patients with Alzheimer's Disease

Ciaramella

Bizzoni

Salani

et al. 2010

JAD

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Abstract. Alzheimer's disease (AD) is characterized by abnormal accumulation of amyloid-β peptide (Aβ) into extracellular fibrillar deposits, paralleled by chronic neuroinflammatory processes. Although Aβ seems to be causative in AD brain damage, the role of the immune system and its mechanisms still remain to be clarified. We have recently shown that normal monocyte-derived dendritic cells (MDDCs), when differentiated in the presence of Aβ1−42, acquire an inflammatory phenotype and a reduced antigen presenting ability. Here we studied MDDCs derived from AD patients in comparison with MDDCs obtained from healthy control subjects (HC). MDDCs from AD patients, at variance with HC-derived cells, were characterized by an augmented cell recovery, a consistent increase in the expression of the pro-inflammatory ICAM-1 molecule, a decrease in the expression of the co-stimulatory CD40 molecule, and an impaired ability to induce T cell proliferation. Furthermore, MDDCs from AD produced higher amounts of IL-6 than HC-derived cells, confirming the more pronounced pro-inflammatory features of these cells in AD patients. Consistent results have been also obtained with monocytes, the MDDC precursors. In fact, while unstimulated monocytes do not appear to be different in AD and HC, after stimulation with lipopolysaccharide, AD monocytes overexpressed ICAM-1 with respect to controls, suggesting that common pathways of monocyte activation and MDDC differentiation are altered in AD. Overall, these findings show that AD-linked dysregulated immune mechanisms exist, which lead to dendritic cell-mediated over-activation of inflammation and impaired antigen presentation, thus supporting the view that immune cell activation could play an important role in AD pathogenesis.

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The role of soluble intercellular adhesion molecules in neurodegenerative disorders

Cited by 45 publications

References 56 publications

Markers of endothelial dysfunction in older subjects with late onset Alzheimer's disease or vascular dementia

Markers of endothelial dysfunction in older subjects with late onset Alzheimer's disease or vascular dementia

Reduced plasma levels of P-selectin and L-selectin in a pilot study from Alzheimer disease: relationship with neuro-degeneration

Increased Pro-Inflammatory Response by Dendritic Cells from Patients with Alzheimer's Disease

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