Impaired cognitive function in Crohn’s disease: Relationship to disease activity

Abstract

Background & aims Impaired attention and response inhibition have been reported in patients with Crohn’s disease (CD) in clinical remission. Prospective studies are needed to determine whether this is a stable feature of CD and whether a similar impairment is evident in ulcerative colitis (UC). Thus, our aims were to examine whether patients with CD and UC exhibited a persistent impairment in attentional performance, and if this impairment was related to key biological indices of relevance to cognition. Methods A prospective observational study was conducted on fifteen patients with CD and 7 with UC in clinical remission recruited from a specialty clinic and 30 healthy matched control participants. A neuropsychological assessment was carried out at baseline (visit 1) and at a 6 month follow-up (visit 2). Plasma proinflammatory cytokines, the plasma kynurenine:tryptophan (Kyn:Trp) ratio and the salivary cortisol awakening response (CAR) were also determined at each visit. Results Across visits, patients with CD exhibited impaired attentional performance ( p ​= 0.023). Plasma IL-6 ( P ​= ​0.001) and the Kyn:Trp ratio ( P ​= ​0.03) were consistently elevated and the CAR significantly blunted ( P ​< ​0.05) in patients with CD. No significant relationships were identified between any biochemical parameter and altered cognitive performance. Conclusions Impaired cognitive function is a stable feature of patients with CD. These data suggest that even where remission has been achieved, the functional impact of an organic gastrointestinal disorder on cognition is still evident. However, it is unclear at present if physiological changes due to disease activity play a role in cognitive impairment in CD.

Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits

“…TBI and DSS-induced colitis are reported to alter social behavior in rodents [ 55 , 56 ]. We next assessed the effect of intestinal inflammation during chronic TBI on social behavior using Crawley’s three-chamber social approach task (SA) 3 weeks after the onset of intestinal inflammation (PTD51-54).…”

“…Deficits in social recognition and memory were reported in pediatric and young adult mice subjected to TBI [ 45 , 56 , 78 ]. Inflammatory bowel disease (IBD) is also associated with neurological dysfunction in patients [ 55 , 79 , 80 ] and is a risk factor for neurodegenerative diseases and neurodevelopmental disorders [ 81 – 84 ]. Rodent models of acute colitis report deficits in working, declarative, and social recognition and memory [ 19 , 22 , 85 ].…”

A fiber-deprived diet causes cognitive impairment and hippocampal microglia-mediated synaptic loss through the gut microbiota and metabolites

“…In the colitis mouse model induced by dextran sodium sulfate, elevated frequencies of inflammatory M1-like microglia, and increased release of pro-inflammatory cytokines are observed in the hippocampus [ 38 ]. In clinical studies, patients with inflammatory bowel disease present with impaired cognitive function and decreased hippocampal activity, as assessed by magnetic resonance imaging [ 39 , 40 ]. In line with this evidence, we found that fiber deficiency impaired colonic homeostasis, including the loss of barrier integrity and inflammation, which is concomitant with the appearance of hippocampal neuroinflammation and synaptic impairment, indicating a perturbed gut-brain axis.…”

Heart-brain connections: phenotypic and genetic insights from 40,000 cardiac and brain magnetic resonance images

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