ABCB1 (MDR1), APOE, BDNF, CNR1, COMT, DAT1 (SLC6A3), DRD4, ESR1, HLA-DRB1, IL10, IL1B, IL6, LTA, PTGS2 (COX-2), SLC6A4, and TNF were associated with cognitive impairment and pain, which had the most genes in common.
Cytokines such as TNFα play an integral role in sleep/wake regulation and have recently been hypothesized to be involved in cognitive impairment due to sleep deprivation.
Early elevations of C-reactive protein, tumor necrosis factor-α, interleukin (IL)-8, intercellular adhesion molecule (ICAM)-1, and erythropoietin were associated with IQ values >2 SD below the expected mean (ORs: 2.0-2.3) and with moderate to severe cognitive impairment on a composite measure of IQ and executive function (ORs: 2.1-3.6).
Early intervention with a small molecule inhibitor for tumor necrosis factor-α prevents cognitive deficits in a triple transgenic mouse model of Alzheimer's disease.
Finally, dexamethasone protects against the two hit mediated cognitive impairment by lowering the pro-inflammatory factors (TNF-α/IL-1β) both in lungs and blood.
In addition, IL-1and TNF-α were downregulated, while IL-6 and SOD were upregulated in patients with cognitive dysfunction after treatment with DEX compared with those in the placebo group.
In conclusion, fish and flaxseed oils exerted a protective effect on cognitive impairment and decreased the incidence of depressive-like behavior in d-gal- and sucrose-fed prediabetic aging rats. n-3 PUFA-rich oil diets, particularly the fish oil diet, reduced the plasma levels of nonesterified fatty acids, tumor necrosis factor-α, and brain dopamine and RAGE expression but not glycemic status, resulting in an improvement in the time of escape latency and the time spent in the target quadrant in the MWM test.
In this study, the effect of SAK on spatial discrimination in a rat model of cognitive dysfunction exposed to D-galactose was investigated with respect to its effect on malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels, and on the expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nuclear factor-κB inhibitory factor-α (IκBα) in hippocampus of rats.
Inflammatory cytokine levels, including interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF) α, in the blood have been associated with cognitive impairment and decline.However, evidence has been mixed.
Interestingly, daily intraperitoneal administration of galantamine, an inhibitor of acetylcholinesterase, reversed cognitive dysfunction in surgery mice and attenuated accumulation of microglia and protein levels of IL-1β, IL-6 and TNF-α in the hippocampus.
LPS caused a marked elevation in IL-1β and TNF-α levels both peripherally and in the brain, together with microglia activation (p < 0.05) and cognitive impairment.
Multifunctional Compound AD-35 Improves Cognitive Impairment and Attenuates the Production of TNF-α and IL-1β in an Aβ25-35-induced Rat Model of Alzheimer's Disease.
Our findings provided preliminary evidence that the interaction of BDNF and TNF-α may confer susceptibility to schizophrenia and cognitive dysfunction.
Our results exhibited that CB treatment prevented cognitive impairment, Aβ deposits, microglia activation and production of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the brain of APP/PS1 mice.
Our results suggest that TNF-α is associated with cognitive and functional decline and that inflammation could be a substrate of cognitive impairment at early clinical stages of dementia.
Our results suggest that the SNP -1031T>C of the TNF-alpha gene may not be associated with susceptibility to schizophrenia but possibly acts as a modulator for its onset age as well as for cognitive deficits.
Plasma levels of soluble CD14 and tumor necrosis factor-alpha type II receptor correlate with cognitive dysfunction during human immunodeficiency virus type 1 infection.
Rats with KA-induced seizures showed longer average escape latency and decreases in the number of platform crossings and average time spent in the target quadrant in the Morris water maze; ISL pretreatment reversed this decline in cognitive impairment and increased the protein levels of synaptophysin, postsynaptic density-95 and brain-derived neurotrophic factor while reducing the number of Fluoro Jade B-positive cells, microglia, and astrocytes; cleaved-Caspase-3 and -9 protein levels; and tumor necrosis factor-α, interleukin (IL)-1β, and IL-18 production.
Serum levels of IL-15, CXCL10, CCL22 and TNF-α were significantly associated with cognitive decline, suggesting a peripheral inflammatory response to neurodegeneration.