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Sökning: WFRF:(Rolstad Sindre 1976) > (2015-2019) > Johansson Boo

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1.
  • Eckerström, Marie, 1981, et al. (författare)
  • Longitudinal evaluation of criteria for subjective cognitive decline and preclinical Alzheimer's disease in a memory clinic sample.
  • 2017
  • Ingår i: Alzheimer's & Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 16:8, s. 96-107
  • Tidskriftsartikel (refereegranskat)abstract
    • Subjective cognitive decline (SCD) and biomarker-based "at-risk" concepts such as "preclinical" Alzheimer's disease (AD) have been developed to predict AD dementia before objective cognitive impairment is detectable. We longitudinally evaluated cognitive outcome when using these classifications.Memory clinic patients (n=235) were classified as SCD (n=122): subtle cognitive decline (n=36) and mild cognitive impairment (n=77) and subsequently subclassified into SCDplus and National Institute on Aging-Alzheimer's Association (NIA-AA) stages 0 to 3. Mean (standard deviation) follow-up time was 48 (35) months. Proportion declining cognitively and prognostic accuracy for cognitive decline was calculated for all classifications.Among SCDplus patients, 43% to 48% declined cognitively. Among NIA-AA stage 1 to 3 patients, 50% to 100% declined cognitively. The highest positive likelihood ratios (+LRs) for subsequent cognitive decline (+LR 6.3), dementia (+LR 3.4), and AD dementia (+LR 6.5) were found for NIA-AA stage2.In a memory clinic setting, NIA-AA stage 2 seems to be the most successful classification in predicting objective cognitive decline, dementia, and AD dementia.
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2.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Differential Impact of Neurofilament Light Subunit on Cognition and Functional Outcome in Memory Clinic Patients with and without Vascular Burden
  • 2015
  • Ingår i: Journal of Alzheimers Disease. - : IOS Press. - 1387-2877 .- 1875-8908. ; 45:3, s. 873-881
  • Tidskriftsartikel (refereegranskat)abstract
    • The neurofilament light (NF-L) subunit is mainly expressed in large-caliber myelinated axons, and elevated concentrations in the cerebrospinal fluid (CSF) are correlated with damage to white matter and subcortical regions. Because the correlation between NF-L and cognition and functional impairment is largely unknown, we investigated associations in patients (n = 622) with (n = 199) and without (n = 423) vascular burden in subjective cognitive impairment (SCI, n = 168), mild cognitive impairment (MCI, n = 261), and dementia (n = 193). Patients were staged according to disease severity and the presence/absence of cerebrovascular disease. CSF amyloid-beta(1-42) (A beta(1-42))was included in all models due to its concomitant influence on vascular and primary etiology. Linear regression was used to assess associations between NF-L and A beta(1-42) and five cognitive domains of a comprehensive neuropsychological battery as well as with functional impairment using the Clinical Dementia Rating. Changes in these outcomes at the 2-year follow-up were also evaluated. In SCI and MCI patients with vascular burden, higher NF-L concentrations were associated with baseline cognitive performance (beta = -0.38 to -0.58) and executive decline (beta = -0.44). Lower A beta(1-42) levels were associated with worse cognitive performance in dementia (beta = 0.46 to 0.51). In MCI and dementia patients without vascular burden, higher NF-L (beta = -0.30 to -0.34) and lower A beta(1-42) concentrations (beta = 0.30) were associated with reduced cognitive performance. Higher NF-L concentrations (beta = -0.26) were associated with functional decline in patients with vascular burden. CSF NF-L is associated with cognition in patients with and without vascular etiology. These associations were greater in pre-dementia phases in those with vascular etiology and vice versa in those without vascular burden.
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