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Targeting inflammation in people with schizophrenia could lead to improvements in daily functioning, a study by Sophia Kogan, MD, PhD, and her associates at the Icahn School of Medicine at Mount Sinai, New York, has suggested.
“Our findings invite speculation about the underlying link between inflammation and neurocognitive dysfunction in schizophrenia,” Dr. Kogan and her associates wrote in Brain, Behavior, and Immunity. “Our results suggest that these associations also extend to poor daily functioning in this population.”
to analyze neurocognition, functions of daily living, and inflammatory markers in 41 adults aged 18-55 years with schizophrenia, schizoaffective disorder, or psychosis. Among the individuals in the trial, 36% were female, the average age was 37 years, and the average body mass index was 31 kg/m2. In addition, all of the individuals were either taking antipsychotics or were on doses of injectable depot antipsychotics. People with active substance use and mild depressive symptoms were excluded.
Dr. Kogan and her associates found that poorer neurocognition was tied to increased levels of peripheral tumor necrosis factor–alpha (TNF-a) and interleukin-12 (IL-12p70).
“For TNF-a, these findings were driven primarily by significant associations with poorer neurocognitive performance in the domains of speed of processing (P = .02), visual learning (P = .02), and reasoning and problem solving (P = .03),” wrote Dr. Kogan and her associates. “Similarly, the association between neurocognition and IL-12p70 was driven primarily by decreased speed of processing (P less than .01) and visual learning (P = .05).”
The small sample size was cited as a limitation, as was the exclusion of people with substance use and mild depressive symptoms.
The National Institute of Mental Health funded the study. Dr. Kogan reported no conflicts of interest. Coauthor David Kimhy, PhD, is a consultant to NeuroCog Trials relating to another project.
SOURCE: Kogan S et al. Brain Behav Immun. 2018 Sep 12. doi: 10.1016/j.bbi.2018.09.016.
Targeting inflammation in people with schizophrenia could lead to improvements in daily functioning, a study by Sophia Kogan, MD, PhD, and her associates at the Icahn School of Medicine at Mount Sinai, New York, has suggested.
“Our findings invite speculation about the underlying link between inflammation and neurocognitive dysfunction in schizophrenia,” Dr. Kogan and her associates wrote in Brain, Behavior, and Immunity. “Our results suggest that these associations also extend to poor daily functioning in this population.”
to analyze neurocognition, functions of daily living, and inflammatory markers in 41 adults aged 18-55 years with schizophrenia, schizoaffective disorder, or psychosis. Among the individuals in the trial, 36% were female, the average age was 37 years, and the average body mass index was 31 kg/m2. In addition, all of the individuals were either taking antipsychotics or were on doses of injectable depot antipsychotics. People with active substance use and mild depressive symptoms were excluded.
Dr. Kogan and her associates found that poorer neurocognition was tied to increased levels of peripheral tumor necrosis factor–alpha (TNF-a) and interleukin-12 (IL-12p70).
“For TNF-a, these findings were driven primarily by significant associations with poorer neurocognitive performance in the domains of speed of processing (P = .02), visual learning (P = .02), and reasoning and problem solving (P = .03),” wrote Dr. Kogan and her associates. “Similarly, the association between neurocognition and IL-12p70 was driven primarily by decreased speed of processing (P less than .01) and visual learning (P = .05).”
The small sample size was cited as a limitation, as was the exclusion of people with substance use and mild depressive symptoms.
The National Institute of Mental Health funded the study. Dr. Kogan reported no conflicts of interest. Coauthor David Kimhy, PhD, is a consultant to NeuroCog Trials relating to another project.
SOURCE: Kogan S et al. Brain Behav Immun. 2018 Sep 12. doi: 10.1016/j.bbi.2018.09.016.
Targeting inflammation in people with schizophrenia could lead to improvements in daily functioning, a study by Sophia Kogan, MD, PhD, and her associates at the Icahn School of Medicine at Mount Sinai, New York, has suggested.
“Our findings invite speculation about the underlying link between inflammation and neurocognitive dysfunction in schizophrenia,” Dr. Kogan and her associates wrote in Brain, Behavior, and Immunity. “Our results suggest that these associations also extend to poor daily functioning in this population.”
to analyze neurocognition, functions of daily living, and inflammatory markers in 41 adults aged 18-55 years with schizophrenia, schizoaffective disorder, or psychosis. Among the individuals in the trial, 36% were female, the average age was 37 years, and the average body mass index was 31 kg/m2. In addition, all of the individuals were either taking antipsychotics or were on doses of injectable depot antipsychotics. People with active substance use and mild depressive symptoms were excluded.
Dr. Kogan and her associates found that poorer neurocognition was tied to increased levels of peripheral tumor necrosis factor–alpha (TNF-a) and interleukin-12 (IL-12p70).
“For TNF-a, these findings were driven primarily by significant associations with poorer neurocognitive performance in the domains of speed of processing (P = .02), visual learning (P = .02), and reasoning and problem solving (P = .03),” wrote Dr. Kogan and her associates. “Similarly, the association between neurocognition and IL-12p70 was driven primarily by decreased speed of processing (P less than .01) and visual learning (P = .05).”
The small sample size was cited as a limitation, as was the exclusion of people with substance use and mild depressive symptoms.
The National Institute of Mental Health funded the study. Dr. Kogan reported no conflicts of interest. Coauthor David Kimhy, PhD, is a consultant to NeuroCog Trials relating to another project.
SOURCE: Kogan S et al. Brain Behav Immun. 2018 Sep 12. doi: 10.1016/j.bbi.2018.09.016.
FROM BRAIN, BEHAVIOR, AND IMMUNITY