Peripheral Inflammatory Response in Alzheimer's Disease and Multiinfarct Dementia

Luigi, Ada De; Pizzimenti, Simone; Quadri, Pierluigi; Lucca, Ugo; Tettamanti, Mauro; Fragiacomo, C.; Simoni, Maria Grazia De

doi:10.1006/nbdi.2002.0556

Cited by 59 publications

(44 citation statements)

References 40 publications

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“…Similarly, we did not find any significant difference in IL-1β production between elderly controls, MCI and mild AD subjects. TNF-α and IL-6 release from blood cells stimulated with LPS was shown to be downregulated in AD (De Luigi et al, 2002). This is in agreement with our findings that TNF-α/IL-10 and IL-6/IL-10 ratios were lower in MCI compared to controls, showing that depressed production of these proinflammatory cytokines with respect to IL-10 in LPS but not PHA stimulated PBMCs can be detected early in the preclinical stage of AD.…”

Section: Discussionsupporting

confidence: 92%

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Increased production of inflammatory cytokines in mild cognitive impairment

Magaki

Mueller

Dickson

et al. 2007

Experimental Gerontology

138

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Recent studies indicate that chronic inflammation plays a pathogenic role in both the central nervous system (CNS) and periphery in Alzheimer's disease (AD). We have screened for cytokines differentially produced by peripheral blood mononuclear cells (PBMCs) isolated from subjects with mild cognitive impairment (MCI) and mild AD subjects who had progressed from MCI using a commercially available cytokine array. Following determination of expressed cytokines, we quantified levels of the proinflammatory cytokines TNF-α, IL-6, and IL-8, and the antiinflammatory cytokine IL-10 using flow cytometry. We have found a significant increase in the levels of IL-6, IL-8, and IL-10 produced by PBMCs stimulated for 24 hours with phytohemagglutinin (PHA) in MCI subjects compared to healthy elderly controls. However, in PBMCs stimulated for 48 h with lipopolysaccharide (LPS), lower TNF-α/IL-10, IL-6/IL-10, and IL-8/IL-10 ratios were seen in MCI subjects. There were no differences in plasma levels of IL-8 between aged controls, MCI, and mild AD, and the levels of circulating IL-6 and IL-10 were below detection limits. Our data indicate that changes in cytokine production by PBMCs may be detected early in MCI, and an alteration of the immune response may precede clinical AD.

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Section: Discussionsupporting

confidence: 92%

“…Statistical analysis was performed using the SPSS 12.0.1 software. Since cytokines are known to have a non-Gaussian distribution (De Luigi et al, 2002;Lombardi et al, 1999), differences among cytokine production were evaluated using the non-parametric Mann-Whitney U test. A P value of <0.05 was chosen to indicate significance.…”

Section: Discussionmentioning

confidence: 99%

Increased production of inflammatory cytokines in mild cognitive impairment

Magaki

Mueller

Dickson

et al. 2007

Experimental Gerontology

138

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“…It is a prototypic proinflammatory cytokine and a key regulator of local tissue responses to injury and disease in the CNS [28]. Our results confirm previous findings documenting increased levels of IL-1β in brain lesions, CSF [28,29], and blood of AD patients [6,19,30,31,32,33,34]. IL-1β is supposed to have both beneficial and detrimental effects on the AD pathogenesis.…”

Section: Discussionsupporting

confidence: 81%

Serum Interleukin-10 Levels Correlate with Cerebrospinal Fluid Amyloid Beta Deposition in Alzheimer Disease Patients

D’Anna

Abu‐Rumeileh²,

Fabris³

et al. 2017

Neurodegener Dis

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Background and Objective: In Alzheimer disease (AD) inflammation becomes evident throughout the course of the disease. However, the association between inflammation, cognitive impairment, and cerebrospinal biomarkers (Aβ42, t-tau, p-tau181, and Aβ42/p-tau181 ratio) is poorly understood. Methods: A large panel of inflammatory cytokines (interleukin [IL]-1β, IL-1ra, IL-2, IL-4, IL-6, IL-10, IL-17, interferon-γ, tumor necrosis factor-α, and vascular endothelial growth factor) was analyzed using a multiplex immunoassay in 27 patients with a diagnosis of AD dementia and in 18 control subjects. In a subgroup with available cerebrospinal fluid (CSF) samples, cytokines in serum were correlated with the levels of neurodegenerative CSF biomarkers (Aβ42, t-tau, p-tau181, and Aβ42/p-tau181 ratio). Results: Compared to control subjects, AD patients showed a significant upregulation of IL-10, IL-1β, and IL-17 serum levels. Several cytokines appeared intercorrelated, and IL-10 in particular presented a significant inverse correlation with CFS levels of Aβ42 and the Aβ42/p-tau ratio. Conclusion: Our findings indicate that serum levels of IL-10 may represent a possible peripheral expression of amyloid beta deposition in AD patients.

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“…This, in effect, is a measure of an individual's intrinsic cytokine producing ability following a controlled stimulus. Using this approach a number of cross sectional studies [33][34][35] have shown an increase in the intrinsic production of proinflammatory cytokines in AD subjects compared with controls; although not all [36]. More recently, a prospective study [37] suggested that cognitively intact individuals in the top tertile of PBMC TNFα (or IL-1β) production have an approximately three times increased risk of developing AD compared with those in the lowest tertile.…”

Section: The Immune System In Alzheimer's Disease the Systemic Immunementioning

confidence: 99%

Systemic and Central Immunity in Alzheimer's Disease: Therapeutic Implications

Butchart

Holmes

2011

CNS Neuroscience & Therapeutics

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SUMMARYClinical pharmaceutical trials aimed at modulating the immune system in Alzheimer's Disease have largely focused on either dampening down central proinflammatory innate immunity or have manipulated adaptive immunity to facilitate the removal of centrally deposited beta amyloid. To date, these trials have had mixed clinical therapeutic effects. However, a number of clinical studies have demonstrated disturbances of both systemic and central innate immunity in Alzheimer's Disease and attention has been drawn to the close communication pathways between central and systemic immunity. This paper highlights the need to take into account the potential systemic effects of drugs aimed at modulating central immunity and the possibility of developing novel therapeutic approaches based on the manipulation of systemic immunity and its communication with the central nervous system.

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Peripheral Inflammatory Response in Alzheimer's Disease and Multiinfarct Dementia

Cited by 59 publications

References 40 publications

Increased production of inflammatory cytokines in mild cognitive impairment

Increased production of inflammatory cytokines in mild cognitive impairment

Serum Interleukin-10 Levels Correlate with Cerebrospinal Fluid Amyloid Beta Deposition in Alzheimer Disease Patients

Systemic and Central Immunity in Alzheimer's Disease: Therapeutic Implications

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