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.
The triangle of death of neurons: Oxidative damage, mitochondrial dysfunction, and loss of choline-containing biomolecules in brains of mice treated with doxorubicin. Advanced insights into mechanisms of chemotherapy induced cognitive impairment ("chemobrain") involving TNF-α.
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.
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.
These results suggest that the transient upregulation of microglia and TNFα in the mPFC induced by adolescent social stress may participate in the development of cognitive flexibility deficit and that immunomodulation may act as a potential target for the early prevention of cognitive deficits in psychiatric disorders.
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.
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.
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.
The increase of TNF-α and IL-6 expression might trigger the disruption of BBB in the brain, which eventually caused cognitive impairment in the 8-week STZ rats.
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.
Single studies suggest the role of CRP, interleukin(IL)-1 receptor antagonist, IL-6 and TNF-α with its receptors in the development of cognitive impairment in BD.
Various pro-inflammatory cytokines, such as TNFα, maintain a state of chronic neuroinflammation, manifesting as post-operative cognitive dysfunction and post-operative delirium.
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.
The potential for exercise to regulate human TNF and TNF signalling and cognitive dysfunction needs investigation under inflammatory conditions including depression and neuropsychiatric disorders.
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.
Our findings provided preliminary evidence that the interaction of BDNF and TNF-α may confer susceptibility to schizophrenia and cognitive dysfunction.
Serum levels of IL-15, CXCL10, CCL22 and TNF-α were significantly associated with cognitive decline, suggesting a peripheral inflammatory response to neurodegeneration.
The present study investigates the potential of trans-Sinapic Acid as neuromodulator and its effect on release of Monoamine Oxidase (MAO-A, MAO-B), TNF-α, Acetylcholine esterase Enzyme, in cognitive dysfunctions associated with experimental dementia.
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.
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.
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.