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Träfflista för sökning "WFRF:(Rolstad Sindre 1976) "

Sökning: WFRF:(Rolstad Sindre 1976)

  • Resultat 1-10 av 45
  • [1]2345Nästa
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1.
  • Abé, C, et al. (författare)
  • Bipolar disorder type I and II show distinct relationships between cortical thickness and executive function.
  • 2018
  • Ingår i: Acta psychiatrica Scandinavica. - 1600-0447. ; 138:4, s. 325-335
  • Tidskriftsartikel (refereegranskat)abstract
    • Frontal cortical abnormalities and executive function impairment co-occur in bipolar disorder. Recent studies have shown that bipolar subtypes differ in the degree of structural and functional impairments. The relationships between cognitive performance and cortical integrity have not been clarified and might differ across patients with bipolar disorder type I, II, and healthy subjects.Using a vertex-wise whole-brain analysis, we investigated how cortical integrity, as measured by cortical thickness, correlates with executive performance in patients with bipolar disorder type I, II, and controls (N = 160).We found focal associations between executive function and cortical thickness in the medial prefrontal cortex in bipolar II patients and controls, but not in bipolar I disorder. In bipolar II patients, we observed additional correlations in lateral prefrontal and occipital regions.Our findings suggest that bipolar disorder patients show altered structure-function relationships, and importantly that those relationships may differ between bipolar subtypes. The findings are line with studies suggesting subtype-specific neurobiological and cognitive profiles. This study contributes to a better understanding of brain structure-function relationships in bipolar disorder and gives important insights into the neuropathophysiology of diagnostic subtypes.
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2.
  • Eckerström, Marie, 1981, et al. (författare)
  • Sahlgrenska Academy Self-reported Cognitive Impairment Questionnaire (SASCI-Q) - a research tool discriminating between subjectively cognitively impaired patients and healthy controls.
  • 2013
  • Ingår i: International psychogeriatrics / IPA. - 1741-203X. ; 25:3, s. 420-430
  • Tidskriftsartikel (refereegranskat)abstract
    • ABSTRACT Background: Subjective cognitive impairment (SCI) is a potential early marker for actual cognitive decline. The cognitive manifestation of the SCI stage is, however, largely unknown. Self-report instruments developed especially for use in the SCI population are lacking, and many SCI studies have not excluded mild cognitive impairment and dementia. We developed and tested a patient-based questionnaire on everyday cognitive function aiming to discriminate between patients with subjective, but not objective, cognitive impairment and healthy controls. Methods: Individuals experiencing cognitive impairment were interviewed to generate a pool of items. After condensing to 97 items, we tested the questionnaire in 93 SCI patients seeking care at a memory clinic (age M = 64.5 years, Mini-Mental State Examination (MMSE) M = 29.0) and 50 healthy controls (age M = 69.6 years, MMSE M = 29.3). Further item reduction was conducted to maximize that remaining items would discriminate between SCI patients and controls, using a conservative α level and requiring medium to high effect sizes. Internal consistency reliability and convergent validity was subsequently examined. Results: Forty-five items discriminated between the groups, resulting in the Sahlgrenska Academy Self-reported Cognitive Impairment Questionnaire (SASCI-Q). Internal consistency was high and correlations to a single question on memory functioning were of medium to large sizes. Most remaining items were related to the memory domain. Conclusion: The SASCI-Q discriminates between SCI patients and healthy controls and demonstrates satisfying psychometric properties. The instrument provides a research method for examining SCI and forms a foundation for future examining which SCI symptoms predict objective cognitive decline. The cognitive manifestation of the SCI stage is mostly related to experiences of memory deficits.
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3.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Cognitive Performance and Cerebrospinal Fluid Biomarkers of Neurodegeneration: A Study of Patients with Bipolar Disorder and Healthy Controls
  • 2015
  • Ingår i: Plos One. - 1932-6203. ; 10:5
  • Tidskriftsartikel (refereegranskat)abstract
    • The purpose of the present study was to investigate if cerebrospinal fluid (CSF) biomarkers of neurodegeneration are associated with cognition in bipolar disorder and healthy controls, respectively. CSF concentrations of total and phosphorylated tau, amyloid beta (A beta) 1-42, ratios of A beta 42/40 and A beta 42/38, soluble amyloid precursor protein alpha and beta, and neurofilament light chain protein were analyzed in relation to neuropsychological performance in 82 euthymic bipolar disorder patients and 71 healthy controls. Linear regression models were applied to account for performance in five cognitive domains using the CSF biomarkers. In patients, the CSF biomarkers explained a significant proportion of the variance (15-36%, p =. 002 -<. 0005) in all cognitive domains independently of age, medication, disease status, and bipolar subtype I or II. However, the CSF biomarkers specifically mirroring Alzheimer-type brain changes, i.e., P-tau and A beta 1-42, did not contribute significantly. In healthy controls, CSF biomarkers did not explain the variance in cognitive performance. Selected CSF biomarkers of neurodegenerative processes accounted for cognitive performance in persons with bipolar disorder, but not for healthy controls. Specifically, the ratios of A beta 42/40 and A beta 42/38 were consistently associated with altered cognitive performance.
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4.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Cognitive reserve lessens the burden of white matter lesions on executive functions in bipolar disorder
  • 2016
  • Ingår i: Psychological Medicine. - 0033-2917 .- 1469-8978. ; 46:15, s. 3095-3104
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. The concept of cognitive reserve (CR) hypothesizes that intellectually stimulating activities provide resilience against brain pathology/disease. Whereas brain abnormalities and cognitive impairment are frequently reported in bipolar disorder (BD), it is unknown whether the impact of brain alterations can be lessened by higher CR in BD. Method. We tested if higher CR would reduce the influence of total volumes of deep white matter hypointensities (WMH), ventricular cerebrospinal fluid (CSF), and prefrontal cortex on memory, executive, and attention/speed functions in patients with BD (n = 75). Linear regression models with interaction terms for CR and brain volumes were applied to directly test if CR reduces the influence of brain pathology on cognitive domains. Results. CR reduced the influence of total volumes of deep WMH (beta=-0.38, Q = 0.003) and ventricular CSF (beta = -41, Q = 006) on executive functions. Conclusions. The interactions between CR and total volumes of deep WMH/ventricular CSF appear to account for executive functioning in BD. The results suggest that the concept of CR is applicable in BD. Higher reserve capacity in BD alters the relationship between brain pathology and clinical presentation.
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5.
  • Rolstad, Sindre, 1976, et al. (författare)
  • CSF neuroinflammatory biomarkers in bipolar disorder are associated with cognitive impairment.
  • 2015
  • Ingår i: European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. - 1873-7862. ; 25:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Persistent cognitive impairment in the euthymic state of bipolar disorder is increasingly recognized. Mounting evidence also suggests an association between neuroinflammation and cognitive dysfunction. The purpose of this study was to test if cerebrospinal fluid (CSF) markers of neuroinflammation could account for cognitive impairment in bipolar disorder. Hierarchical linear regression models were applied to account for performance in five cognitive domains using CSF neuroinflammatory biomarkers as predictors in patients with bipolar disorder type I and II (N=78). The associations between these biomarkers and cognition were further tested in healthy age- and sex-matched controls (N=86). In patients with bipolar disorder, the CSF biomarkers accounted for a significant proportion of the variance in executive functions (42.8%, p=<.0005) independently of age, medication, disease status, and bipolar subtype. The microglial marker YKL-40 had a high impact (beta=-.99), and was the only biomarker that contributed individually. CSF biomarkers were not associated with cognitive performance in healthy controls. The CSF neuroinflammation biomarker YKL-40 is associated with executive performance in euthymic bipolar disorder, but not in healthy controls.
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6.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Polymorphisms of BDNF and CACNA1C are not associated with cognitive functioning in bipolar disorder or healthy controls.
  • 2016
  • Ingår i: Cognitive neuropsychiatry. - 1464-0619. ; 21:3, s. 271-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The cause of cognitive dysfunction in bipolar disorder (BD) is not well understood. BDNF and CACNA1C are two susceptibility genes for the disorder that have also been reported to be associated with cognitive deficits in the disorder, but the studies have been small and with conflicting results. We therefore attempted to replicate an association between cognitive dysfunction with the most commonly studied single nucleotide polymorphisms rs6265 and rs1006737.
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7.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Polymorphisms of dopamine pathway genes NRG1 and LMX1A are associated with cognitive performance in bipolar disorder
  • 2015
  • Ingår i: Bipolar disorders. - 1399-5618. ; 17:8
  • Tidskriftsartikel (refereegranskat)abstract
    • LIM homeobox transcription factor 1, alpha (LMX1A) and neuregulin 1 (NRG1) are susceptibility genes for schizophrenia that have been implicated in the dopaminergic pathway and have been associated with altered cognitive functioning. We hypothesized that single nucleotide polymorphisms (SNPs) in LMX1A and NRG1 would be associated with cognitive functioning in bipolar disorder.
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8.
  • Balogh, Nora, et al. (författare)
  • The five-items memory screen-extended variant: A tool for assessing memory
  • 2020
  • Ingår i: Acta Neurologica Scandinavica. - 0001-6314. ; 141:2, s. 162-167
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and purpose The detection of memory impairment is an important part of dementia screening. However, the scope of memory measures in current screening batteries is limited. There is a need for a short yet sensitive instrument for early detection of memory impairment that could serve as a complement to existing globally oriented screening tests, for example, Mini-Mental State Examination (MMSE). To that end, the current study investigates the sensitivity and psychometric properties of the memory screening instrument The Five-Items Memory Screen -Extended Variant (FIMS-XV). Methods Hundred and forty-five participants included in the Gothenburg Mild Cognitive Impairment Study-27 patients with subjective cognitive impairment (SCI), 73 with mild cognitive impairment (MCI), and 45 with mild dementia-underwent cognitive screening including the MMSE and FIMS-XV. Ninety participants also underwent extensive neuropsychological testing. Results The FIMS-XV showed high internal consistency and strong correlations with established neuropsychological memory tests. Both the FIMS-XVdelayed recall score and the FIMS-XV total score differentiated mild dementia patients from patients with SCI and MCI. Conclusions The FIMS-XV shows promise as a sensitive tool for screening for memory impairment in all putative phases of dementia.
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9.
  • Bjerke, Maria, 1977, et al. (författare)
  • Subcortical vascular dementia biomarker pattern in mild cognitive impairment.
  • 2009
  • Ingår i: Dementia and geriatric cognitive disorders. - 1421-9824. ; 28:4, s. 348-56
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Mild cognitive impairment (MCI) is an etiologically unclear disorder. Cerebrospinal fluid (CSF) biomarkers are potentially useful for the differentiation between various MCI etiologies. AIM: The aim of the study was to assess whether baseline CSF hyperphosphorylated tau (P-tau), total tau (T-tau), amyloid beta 1-42 (Abeta(42)) and neurofilament light (NF-L) in patients with MCI could predict subcortical vascular dementia (SVD) and Alzheimer's disease (AD) at follow-up. METHODS: Biomarker levels were assessed by Luminex xMAP technology and ELISA. RESULTS: Increased baseline concentrations of NF-L significantly separated MCI-SVD from stable MCI. The MCI-SVD patients were inseparable from stable MCI but separable from patients developing AD (MCI-AD) on the basis of Abeta(42,) T-tau and P-tau(181) levels. CONCLUSION: A combination of the biomarkers Abeta(42), T-tau, P-tau(181) and NF-L has the potential to improve the clinical separation of MCI-SVD patients from stable MCI and MCI-AD patients.
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10.
  • Brys, Miroslaw, et al. (författare)
  • Prediction and longitudinal study of CSF biomarkers in mild cognitive impairment.
  • 2009
  • Ingår i: Neurobiology of aging. - 1558-1497. ; 30:5, s. 682-90
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To longitudinally evaluate five cerebrospinal fluid (CSF) biomarkers in the transition from mild cognitive impairment (MCI) to Alzheimer's disease (AD). METHODS: A baseline and 2-year follow-up clinical and CSF study of 86 subjects, including 22 MCI patients that declined to AD (MCI-AD), 43 MCI that did not deteriorate (MCI-MCI) and 21 controls (NL-NL). All subjects were studied for total and phosphorylated tau (T-tau, P-tau(231)), amyloid beta (Abeta) Abeta(42)/Abeta(40) ratio, isoprostane (IP) as well as P-tau(231)/Abeta(42/40) and T-tau/Abeta(42/40) ratios. RESULTS: At baseline and at follow-up MCI-AD showed higher levels P-tau(231), T-tau, IP, P-tau(231)/Abeta(42/40) and T-tau/Abeta(42/40) ratios and lower Abeta(42)/Abeta(40) than MCI-MCI or NL-NL. Baseline P-tau(231) best predicted MCI-AD (80%, p<0.001) followed in accuracy by P-tau(231)/Abeta(42/40) and T-tau/Abeta(42/40) ratios (both 75%, p's<0.001), T-tau (74%, p<0.001), Abeta(42)/Abeta(40) (69%, p<0.01), and IP (68%, p<0.01). Only IP showed longitudinal effects (p<0.05). CONCLUSIONS: P-tau(231) is the strongest predictor of the decline from MCI to AD. IP levels uniquely show longitudinal progression effects. These results suggest the use of CSF biomarkers in secondary prevention trials.
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