Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease

Álvarez, Antón; Cacabelos, Ramón; Sanpedro, Carolina; García-Fantini, Manuel; Aleixandre, Manuel

doi:10.1016/j.neurobiolaging.2006.02.012

Cited by 229 publications

(157 citation statements)

References 19 publications

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“…The data reported in this study are in agreement with the idea that free IGF-I is increased at lung levels (ELF values) in affected infants, further confirmed by decreased PAPP-A levels, which are always inversely correlated in the different models studied (1,10). It has already been reported that tumor necrosis factor-␣ is able to reduce IGF-I and induce the release of PAPP-A molecules (1,10).…”

Section: Epithelial Lining Fluid Levels Of Free Igf-i Papp-a and supporting

confidence: 92%

Epithelial lining fluid free IGF-I-to-PAPP-A ratio is associated with bronchopulmonary dysplasia in preterm infants

Capoluongo

Ameglio

Lulli

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Preterm newborns developing retinopathy of prematurity (ROP) and bronchopulmonary dysplasia (BPD) show persistently low levels of insulin-like growth factor-I (IGF-I) in sera. They also present higher free IGF-I concentrations in epithelial lining fluids (ELFs) and lung tissues. Pregnancy-associated plasma protein-A (PAPP-A) is a metalloproteinase that dissociates three binding proteins from the active form of IGF-I, namely free IGF-I. The present study analyzes the ELF concentrations of free IGF-I, PAPP-A, and their ratios in preterm newborns developing or not BPD, defined as O2 dependence at 36 wk postmenstrual age. Bronchoalveolar lavage fluids of 41 infants (34 without and 7 with BPD) were analyzed on the 2nd and 4th day after birth. Infants developing BPD showed increased ELF free IGF-I and decreased PAPP-A concentrations on both days 2 and 4 compared with newborns without BPD. A nonsignificant trend between these 2 days was observed for free IGF-I (increasing) and PAPP-A (decreasing). On the same days, the free IGF-I-to-PAPP-A ratio was always significantly higher in patients developing BPD. These differences were more significant than those of IGF-I or PAPP-A when individually evaluated. A multivariate analysis confirmed the significance for free IGF-I on day 4, whereas the ratio was confirmed on both days 2 and 4. The same ratio was significantly correlated with some indexes of disease severity, such as hours of oxygen administration, days of hospitalization, and ROP severity scores. Finally, the ratio between ELF free IGF-I and PAPP-A appears to be a useful marker for lung injury of premature newborns.

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Section: Epithelial Lining Fluid Levels Of Free Igf-i Papp-a and supporting

confidence: 92%

Epithelial lining fluid free IGF-I-to-PAPP-A ratio is associated with bronchopulmonary dysplasia in preterm infants

Capoluongo

Ameglio

Lulli

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Raised levels of TNF-a, CRP, IL-6, and IL-12 have repeatedly been found in MCI patients compared with normal controls (Alvarez et al, 2007;Zuliani et al, 2008;Roberts et al, 2009;Trollor et al, 2011). These inflammatory markers were measured in participants' blood samples, collected after an overnight fast, clotted, aliquoted, and frozen at À80°C.…”

Section: Covariatesmentioning

confidence: 99%

“…Several studies have found that inflammatory markers, such as interleukin-6 (IL-6), interleukin-12 (IL-12), tumor necrosis factor-a (TNFa), and C-reactive protein (CRP), are elevated in the elderly and are associated with cognitive impairment and decline (Licastro et al, 2000;Engelhart et al, 2004;Dimopoulos et al, 2006;Alvarez et al, 2007;Zuliani et al, 2008;Trollor et al, 2011), as well as increased risk of mortality .…”

Section: Introductionmentioning

confidence: 99%

Macrophage inhibitory cytokine-1 is associated with cognitive impairment and predicts cognitive decline - the Sydney Memory and Aging Study

et al. 2013

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SummaryHigher levels of macrophage inhibitory cytokine-1, also known as growth differentiation factor 15 (MIC-1/GDF15), are associated with adverse health outcomes and all-cause mortality. The aim of this study was to examine the relationships between MIC-1/GDF15 serum levels and global cognition, five cognitive domains, and mild cognitive impairment (MCI), at baseline (Wave 1) and prospectively at 2 years (Wave 2), in nondemented participants aged 70-90 years. Analyses were controlled for age, sex, education, Framingham risk score, history of cerebrovascular accident, acute myocardial infarction, angina, cancer, depression, C-reactive protein, tumor necrosis factor-a, interleukins 6 and 12, and apolipoprotein e4 genotype. Higher MIC-1/GDF15 levels were significantly associated with lower global cognition at both waves. Cross-sectional associations were found between MIC-1/GDF15 and all cognitive domains in Wave 1 (all P < 0.001) and between processing speed, memory, and executive function in Wave 2 (all P < 0.001). Only a trend was found for the prospective analyses, individuals with high MIC-1/GDF15 at baseline declined in global cognition, executive function, memory, and processing speed. However, when categorizing MIC-1/ GDF15 by tertiles, prospective analyses revealed statistically significant lower memory and executive function in Wave 2 in those in the upper tertile compared with the lower tertile. Receiver operating characteristics (ROC) analysis was used to determine MIC-1/GDF15 cutoff values associated with cognitive decline and showed that a MIC-1/GDF15 level exceeding 2764 pg/ml was associated with a 20% chance of decline from normal to MCI or dementia. In summary, MIC-1/GDF15 levels are associated with cognitive performance and cognitive decline. Further research is required to determine the pathophysiology of this relationship.

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“…Moreover, inflammation and ROS generation are now evident to go hand to hand in a number of pathological manifestations, wherein, TNF-α has been found to play a regulatory role [35,36]. In case of brain disorders also, neuroinflammation and excitotoxicity have been found to be responsible for triggering neuro-excitotoxic disorders/diseases like; traumatic brain injury, Ischemia, Alzheimers disease, Parkinson's disease, etc [17,[37][38][39][40][41][42][43][44][45][46][47]. Recent experimental evidences also suggest that natural antioxidants may modulate the expression of inflammatory cytokines while protecting diseased cells from oxidative insult.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Normalizes Hyperammonemia Induced Pro-Inflammatory and Pro-Apoptotic Conditions in Rat Brain

Khanna¹,

Trigun²

2016

IJCAM

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Research ArticleInt J Complement Alt Med 2016, 4(2): 00115 IntroductionAmmonia neurotoxicity is considered responsible for development of a serious nervous system disorder called hepatic encephalopathy (HE). This situation arises mainly due to liver dysfunction led hyperammonemia (HA). HE is characterized by the neuropsychiatric manifestations related to motor dysfunction, memory impairment, and deranged sleep-awake cycle [1,2]. Since HE affects the quality of life of the patients, it is important to develop effective therapeutic strategy against HE. This necessitates understanding the neuro-chemistry of HA pathogenesis.Since ammonia crosses the blood brain barrier easily, prolonged HA condition, a common situation during chronic liver failure (CLF), is likely to maintain increased ammonia concentration in brain [3,4]. The information, mainly derived from the cell culture system and from animal models with acute HE, suggest that the increased brain ammonia level mainly drives astrocytes to undergo significant morpho-pathological changes and also over activates glutamate-NMDA receptor (N-Methyl-D-Aspartate Receptor) pathway in the post-synaptic neurons [1,[5][6][7]. Moreover, NMDAR inhibition could not be translated into prevention of ammonia neurotoxicity, mainly because threshold glutamate-NMDAR activation is necessary for normal neurological functions including higher order brain functions and normal synaptic activity.During recent past, "TNF theory" (Tumor necrosis factor) of HE pathogenesis could draw much attention due to a close association between the level of TNF-α and ammonia in the brain of CLF patients with HE [8]. Later studies have also emphasized significant involvement of TNF-α and other cytokines in HE to the extent that these cytokines could be used as markers for encephalopathy grading [4,[9][10][11][12][13].It is now evident that the microglia and astroglia cells in brain synthesize TNF-α to regulate higher order brain functions and astrocyte induced synaptic strengthening [14][15][16][17]. However, when produced in higher amounts during neuropathology, they are known to potentiate glutamate induced cytotoxicity by inhibiting glutamate transport to the glial cells from the synaptic cleft [12,[16][17][18][19]. Even development of MHE has been described to be dependent more on enhanced inflammatory markers than the severity of CLF or HA in the CLF patients [20]. Moreover, some findings from in vitro studies suggest that resveratrol treatment could prevent ammonia toxicity in astroglial cells by normalizing ROS/RNS level [12,21,22]. Thus, hinting towards a significant role of resveratrol in ameliorating ammonia toxicity. However, the mechanism by which resveratrol does so is unclear.Resveratrol (3, 3, 4'-trihydroxy-Trans stilbene), a natural polyphenol, is found in a number of dietary sources such as grapes, berries, and red wine [23][24][25]. It acts as an effective cardioprotector, AbstractChronic liver failure (CLF) led hyperammonemia (HA) is known to develop a metabolic brain disorder known a...

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Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease

Cited by 229 publications

References 19 publications

Epithelial lining fluid free IGF-I-to-PAPP-A ratio is associated with bronchopulmonary dysplasia in preterm infants

Epithelial lining fluid free IGF-I-to-PAPP-A ratio is associated with bronchopulmonary dysplasia in preterm infants

Macrophage inhibitory cytokine-1 is associated with cognitive impairment and predicts cognitive decline - the Sydney Memory and Aging Study

Resveratrol Normalizes Hyperammonemia Induced Pro-Inflammatory and Pro-Apoptotic Conditions in Rat Brain

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