Raised Serum Proinflammatory Cytokines in Alzheimer’s Disease with Depression

Khemka, Vineet Kumar; Ganguly, Anirban; Bagchi, Debajit; Ghosh, Arindam; Bir, Aritri; Biswas, Atanu; Chattopadhyay, Sita; Chakrabarti, Sasanka

doi:10.14336/ad.2014.0500170

Cited by 39 publications

(37 citation statements)

References 28 publications

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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: 89%

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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Section: Discussionsupporting

confidence: 89%

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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“…In an earlier study we have observed that AD patients with associated depression have higher circulating levels of pro-inflammatory cytokines than those without depression [44]. In the present study, we have further extended our observation by measuring both pro-inflammatory cytokines and 25-hydroxyvitamin D in circulation in AD patients with or without depression.…”

Section: Discussionsupporting

confidence: 74%

Role of Pro-Inflammatory Cytokines and Vitamin D in Probable Alzheimer's Disease with Depression

Banerjee¹,

Khemka²,

Roy³

et al. 2017

Aging and disease

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Symptoms of depression are present in a significant proportion of Alzheimer's disease (AD) patients. While epidemiological studies have shown a strong association between depression and AD, it has not been established whether depression is a risk factor or merely a co-morbidity of AD. It is also uncertain if depression affects the pathogenesis of AD. In this paper, we address these questions by measuring the serum levels of two common metabolic risk factors of AD and depression, inflammatory cytokines (IL 6 and TNF alpha) and serum 25-hydroxyvitamin D, in a case-control study. We measured the serum levels of IL 6, TNF α and 25-hydroxyvitamin D in age-matched healthy controls (n= 60) and in AD patients without depression (n=26) or AD patients with depression (n=34), and statistically analyzed the changes in these parameters among different groups under this study. Our results show that in AD there is a significant increase in IL 6 and TNF α and a marked decrease in 25-hydroxyvitamin D in the peripheral circulation compared to age-matched healthy controls. Furthermore, AD patients with depression have even significantly higher levels of IL 6 or TNF α and a lower level of 25-hydroxyvitamin D in circulation than in AD patients without depression. We also found a strong statistical correlation between the disease severity and the serum levels of IL 6, TNF α and 25-hydroxyvitamin D in AD patients with depression. These results suggest that altered circulating levels of common metabolic risk factors lead to the co-existence of depression with AD in many patients, and when they co-exist, the depression presumably affects the severity of AD presentations through more aggravated changes in these risk factors.

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“…These results further confirm an imbalance in pro-inflammatory/anti-inflammatory responses in AD. It has been reported that patients with AD have a significant increase in serum IL-1β levels [ 34 , 35 ]. Our present results support and extend the evidence.…”

Section: Discussionmentioning

confidence: 99%

TGF-β1 Protection against Aβ1–42-Induced Neuroinflammation and Neurodegeneration in Rats

Shen

Chen

et al. 2014

IJMS

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Transforming growth factor (TGF)-β1, a cytokine that can be expressed in the brain, is a key regulator of the brain’s responses to injury and inflammation. Alzheimer’s disease (AD), the most common neurodegenerative disorder, involves inflammatory processes in the brain in addition to the hallmarks, amyloid-β (Aβ) plaques and neurofibrillary tangles. Recently, we have shown that T-helper (Th) 17 cells, a subpopulation of CD4+ T-cells with high proinflammation, also participate in the brain inflammatory process of AD. However, it is poorly known whether TGF-β1 ameliorates the lymphocyte-mediated neuroinflammation and, thereby, alleviates neurodegeneration in AD. Herein, we administered TGF-β1 via the intracerebroventricle (ICV) in AD model rats, by Aβ1–42 injection in both sides of the hippocampus, to show the neuroprotection of TGF-β1. The TGF-β1 administration after the Aβ1–42 injection ameliorated cognitive deficit and neuronal loss and apoptosis, reduced amyloid precursor protein (APP) expression, elevated protein phosphatase (PP)2A expression, attenuated glial activation and alleviated the imbalance of the pro-inflammatory/anti-inflammatory responses of T-lymphocytes, compared to the Aβ1–42 injection alone. These findings demonstrate that TGF-β1 provides protection against AD neurodegeneration and suggest that the TGF-β1 neuroprotection is implemented by the alleviation of glial and T-cell-mediated neuroinflammation.

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Raised Serum Proinflammatory Cytokines in Alzheimer’s Disease with Depression

Cited by 39 publications

References 28 publications

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

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

Role of Pro-Inflammatory Cytokines and Vitamin D in Probable Alzheimer's Disease with Depression

TGF-β1 Protection against Aβ1–42-Induced Neuroinflammation and Neurodegeneration in Rats

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