Finally, ATXN1[82Q] transgenic mice-with cerebellum limited expression of mutant ATXN1-demonstrated milder impairment in most aspects of cognition compared to Atxn1154Q/2Q mice, supporting the concept that cognitive deficits in SCA1 arise from a combination of cerebellar and extra-cerebellar dysfunctions.
Here we ask whether chronic IDO1 inhibition by 1-methyl-tryptophan (1-MT, added at 2g/L in the drinking water) or chronic inhibition of tryptophan 2, 3 dioxygenase (TDO2), another enzyme capable of converting tryptophan to kynurenine, by 680C91 (15mg/kg per os), can rescue LPS-induced (0.83mg/kg IP) anxiety and cognitive deficits.
Together, these data suggest that AIE-induced adult neuroimmune signaling and cognitive deficits are linked to suppression of Chat and Trka gene expression through epigenetic mechanisms that can be restored by exercise.
Here we ask whether chronic IDO1 inhibition by 1-methyl-tryptophan (1-MT, added at 2g/L in the drinking water) or chronic inhibition of tryptophan 2, 3 dioxygenase (TDO2), another enzyme capable of converting tryptophan to kynurenine, by 680C91 (15mg/kg per os), can rescue LPS-induced (0.83mg/kg IP) anxiety and cognitive deficits.
We found that FSK and STZ significantly increased the hyperphosphorylated tau level, pyroptosis-related protein in PC12 cell and rats' brain, and inhibited the activity of caspase-1 by caspase-1 inhibitor, caspase-1 siRNA, or incubated with Interleukin(IL)-1β/IL-18 neutralizing antibody could notably alleviate the FSK and STZ induced PC12 cells damage and improve the cognitive disorder in ICV-FSK and ICV-STZ rats.
Both downregulating PKAR2α by shRNA and upregulating proteasome by expressing PA28γ rescued hTau-induced PKA inhibition and CREB dephosphorylation, and upregulating PKA improved hTau-induced cognitive deficits in mice.
Here we show that baseline and learning-induced expression of the growth arrest DNA damage (Gadd45) γ is selectively impaired in the hippocampus of aged mice with cognitive deficits.
In summary, our findings revealed that lncRNA Gm15621 ameliorated the sevoflurane-induced neurotoxicity and the important role of Gm15621/miR-133a/Sox4 axis in cognitive disorder.
Congenital generalized lipodystrophy 2 (CGL2) is characterized by loss of adipose tissue, insulin resistance and cognitive deficits and caused by mutation of BSCL2/seipin gene.
As part of the G-protein coupled receptor (GPCR) family, metabotropic glutamate (mGlu) receptors play an important role as drug targets of cognitive diseases.
However, the relative contribution of COX-2 and COX-1 isoforms in the downstream proinflammatory responses and cognitive deficit in HH remains unknown.
Moreover, we show that heterozygous conditional deletion of ADAM10 or delivery of a competitive TAT-Pro-ADAM10709-729 peptide in R6/2 mice prevents N-CAD proteolysis and ameliorates cognitive deficits in the mice.
As part of the G-protein coupled receptor (GPCR) family, metabotropic glutamate (mGlu) receptors play an important role as drug targets of cognitive diseases.
Our recent study indicates that Casp2-catalyzed tau cleavage at aspartate 314 (tau 2N4R isoform numbering system) mediates synaptotoxicity, cognitive deficits and neurodegeneration in cellular and mouse models of frontotemporal dementia; further, levels of Δtau314, the soluble, N-terminal cleavage product, are elevated in individuals with mild cognitive impairment and Alzheimer's disease, compared with cognitively normal individuals.
However, the relative contribution of COX-2 and COX-1 isoforms in the downstream proinflammatory responses and cognitive deficit in HH remains unknown.