| 1. |
- Nordlund, Arto, 1962, et al.
(författare)
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Cognitive profiles of incipient dementia in the Goteborg MCI study.
- 2010
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Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 30:5, s. 403-10
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Tidskriftsartikel (refereegranskat)abstract
- To study which cognitive profiles of incipient dementia strongest predict the conversion to Alzheimer's disease (AD) and mixed dementia (MD)/vascular dementia (VaD).
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| 2. |
- Nordlund, Arto, 1962, et al.
(författare)
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Two year outcome of MCI subtypes and aetiologies in the Goteborg MCI study.
- 2010
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Ingår i: Journal of neurology, neurosurgery, and psychiatry. - : BMJ. - 1468-330X .- 0022-3050. ; 81:5, s. 541-6
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Tidskriftsartikel (refereegranskat)abstract
- The objective was to study the two year outcome of subjects diagnosed with Mild Cognitive Impairment (MCI). Two hundred and nine subjects diagnosed with MCI were examined with a comprehensive neuropsychological test battery and followed up after two years. After two years 34 subjects (16%) were lost for follow-up. Those subjects did not differ significantly in terms of MCI subclassification, MMSE score or age and education. Of the 175 subjects followed up, 8 (4.5%) had improved to normal, two with amnestic MCI, one from multiple domains MCI, three with single domain MCI and two without any significant impairment at baseline. Forty-four subjects (25%) had progressed to dementia. Out of these 35 were from the multidomain amnestic group and 9 from the multidomain non-amnestic group. The combination of Alzheimer-typical biomarkers (total-tau and amyloid beta) and multidomain amnestic MCI was the strongest predictor of progression to Alzheimer's disease, while vascular disease and multidomain amnestic MCI preceded mixed and vascular dementia. The results suggest that memory impairment alone, or impairment in any one cognitive domain alone, are rather benign conditions. Impairment in several cognitive domains is associated with a more severe outcome over two years. Also, 20% of the subjects who progressed to dementia, including Alzheimer's disease, did not show memory impairment at baseline, which suggests that memory impairment is not always the first symptom of even the most common dementia disorders.
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| 3. |
- Rolstad, Sindre, 1976, et al.
(författare)
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High Education May Offer Protection Against Tauopathy in Patients with Mild Cognitive Impairment.
- 2010
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Ingår i: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 21:1, s. 221-8
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Tidskriftsartikel (refereegranskat)abstract
- The concepts of brain and cognitive reserve stem from the observation that premorbid factors (e.g., education) result in variation in the response to brain pathology. Potential early influence of reserve on pathology, as assessed using the cerebrospinal fluid biomarkers total tau and amyloid-beta{42}, and cognition was explored in mild cognitive impairment (MCI) patients who remained stable over a two-year period. A total of 102 patients with stable MCI grouped on the basis of educational level were compared with regard to biomarker concentrations and cognitive performance. Stable MCI patients with higher education had lower concentrations of t-tau as compared to those with lower education. Also, educational level predicted a significant proportion of the total variance in t-tau concentrations. Our results suggest that higher education may offer protection against tauopathy.
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| 4. |
- Wallin, Anders, 1950, et al.
(författare)
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Progression from mild to pronounced MCI is not associated with cerebrospinal fluid biomarker deviations.
- 2011
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Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 32:3, s. 193-7
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aim: Detection of cerebrospinal fluid (CSF) biomarker deviations improve prediction of progression from mild cognitive impairment (MCI) to dementia. However, it is not settled whether the same pattern exists in patients progressing from very mild to more pronounced MCI. Given that neurodegenerative processes occur very early in the disease course, we also expected to find biomarker deviations in these patients. Methods: A total of 246 memory clinic patients with non-progressive (n = 161), progressive (n = 19), or converting (n = 66) MCI, 67 with stable dementia, and 80 controls were followed for 24 months. At baseline, CSF total tau (T-tau), β-amyloid 1–42 (Aβ42) and the light subunit of neurofilament protein (NFL) were determined. Results: Patients with converting MCI and stable dementia had lower CSF Aβ42 concentrations and higher T-tau concentrations and NFL in comparison with controls and non-progressive/progressive MCI (p < 0.0005). No differences were found between progressive and non-progressive MCI. Conclusion: As expected, biomarker deviations predicted progression from MCI to dementia. Contrary to our hypothesis, progression from very mild MCI to more pronounced MCI was not reflected by biomarker deviations. The results suggest that the measured biomarkers are not early disease markers, or alternatively Alzheimer or vascular pathology is not the underlying cause in this patient group.
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