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.
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.