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- Hooshmand, Babak, et al.
(författare)
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CAIDE Dementia Risk Score, Alzheimer and cerebrovascular pathology : a population-based autopsy study
- 2018
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 283:6, s. 597-603
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Tidskriftsartikel (refereegranskat)abstract
- Background. CAIDE Dementia Risk Score is a tool for estimating dementia risk in the general population. Its longitudinal associations with Alzheimer or vascular neuropathology in the oldest old are not known. Aim. To explore the relationship between CAIDE Dementia Risk Score at baseline and neuritic plaques, neurofibrillary tangles, cerebral infarcts and cerebral amyloid angiopathy (CAA) after up to 10-year follow-up in the Vantaa 85+ population. Methods. Study population included 149 participants aged 85 years, without dementia at baseline, and with available clinical and autopsy data. Methenamine silver staining was used for beta-amyloid and modified Bielschowsky method for neurofibrillary tangles and neuritic plaques. Macroscopic infarcts were identified from cerebral hemispheres, brain-stem and cerebellum slices. Standardized methods were used to determine microscopic infarcts, CAA and alpha-synuclein pathologies. The CAIDE Dementia Risk Score was calculated based on scores for age, sex, BMI, total cholesterol, systolic blood pressure, physical activity and APOE epsilon 4 carrier status (range 0-18 points). Results. A CAIDE Dementia Risk Score above 11 points was associated with more cerebral infarctions up to 10 years later: OR (95% CI) was 2.10 (1.06-4.16). No associations were found with other neuropathologies. Conclusion. In a population of elderly aged 85 years, higher CAIDE Dementia Risk Score was associated with increased risk of cerebral infarcts.
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| 46. |
- Julkunen, V, et al.
(författare)
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Cortical thickness analysis to detect progressive mild cognitive impairment: a reference to Alzheimer's disease
- 2009
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Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 28:5, s. 404-412
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Tidskriftsartikel (refereegranskat)abstract
- <i>Background/Aims:</i> Mild cognitive impairment (MCI) is associated with an increased risk of Alzheimer’s disease (AD). It would be advantageous to be able to distinguish the characteristics of those MCI patients with a high probability to progress to AD if one wishes to monitor the disease development and treatment. <i>Methods:</i> We assessed the baseline MRI and maximum of 7 years clinical follow-up data of 60 MCI subjects in order to examine differences in cortical thickness (CTH) between the progressive MCI (P-MCI) and stable MCI (S-MCI) subjects. CTH was measured using an automatic computational surface-based method. During the follow-up, 15 MCI subjects converted to AD on average 1.9 ± 1.3 years after the baseline examination, while 45 MCI subjects remained stable. <i>Results:</i> The P-MCI group displayed significantly reduced CTH bilaterally in the superior and middle frontal, superior, middle and inferior temporal, fusiform and parahippocampal regions as well as the cingulate and retrosplenial cortices and also in the right precuneal and paracentral regions compared to S-MCI subjects. <i>Conclusions:</i> Analysis of CTH could be used in conjunction with neuropsychological testing to identify those subjects with imminent conversion from MCI to AD several years before dementia diagnosis.
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| 47. |
- Oeckl, P., et al.
(författare)
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Blood beta-synuclein is related to amyloid PET positivity in memory clinic patients
- 2023
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Ingår i: Alzheimers & Dementia. - 1552-5260. ; 19:11, s. 4896-4907
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: beta-synuclein is an emerging blood biomarker to study synaptic degeneration in Alzheimert's disease (AD), but its relation to amyloid-beta (A beta) pathology is unclear. Methods: We investigated the association of plasma beta-synuclein levels with ([18F])flutemetamol positron emission tomography (PET) in patients with AD dementia (n = 51), mild cognitive impairment (MCI-A beta+ n = 18, MCI-A beta-n = 30), non-AD dementias (n = 22), and non-demented controls (n = 5). Results: Plasma beta-synuclein levels were higher in A beta+(AD dementia, MCI-A beta+) than in A beta-subjects (non-AD dementias, MCI-A beta-) with good discrimination of A beta+ from A beta-subjects and prediction of A beta status in MCI individuals. A positive correlation between plasma beta-synuclein and A beta PET was observed in multiple cortical regions across all lobes. Discussion: Plasma beta-synuclein demonstrated discriminative properties for A beta PET positive and negative subjects. Our data underline that beta-synuclein is not a direct marker of A beta pathology and suggest different longitudinal dynamics of synaptic degeneration versus amyloid deposition across the AD continuum.
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