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  • 1
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    Grey zone amyloid burden heralds future memory decline: The SCIENCe Project : Neuroimaging: Novel imaging methods
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S5 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S5 ( 2020-12)
    Abstract: We aimed to compare different thresholds for amyloid‐beta pathology and their associations with memory decline, and to investigate the clinical significance of ‘grey zone’ amyloid‐beta burden in cognitively normal individuals. Method We included 162 cognitively normal participants with subjective cognitive decline (SCD) from the SCIENCe cohort (64±8yr, 38%F, MMSE 29±1). Each underwent a 70‐minutes dynamic [18F]florbetapir PET, T1‐weighted MRI and longitudinal neuropsychological assessment (n=149≥2 visits). PET scans were classified as positive/negative for amyloid pathology by visual assessment (VA). We calculated a mean binding potential (BP ND ) and mean standardized uptake value ratio (SUVr 50‐70 ) for a composite region of interest (orbitofrontal, temporal, anterior/posterior cingulate, precuneus). Using Gaussian mixture modelling and k‐means clustering (2 clusters: 90% of low cluster, 10% of high cluster), we derived 3 thresholds for amyloid positivity (A+) based on both BP ND and SUVr. We compared associations with memory decline for each threshold using linear mixed models (LMM). To investigate whether grey zone amyloid burden is clinically meaningful, we divided the sample into quantiles, and additionally predefined a grey zone using K‐means thresholds (K‐low/K‐grey/K‐high). Result The low K‐means thresholds (BP ND =0.18, SUVr=1.27) were most comparable to VA (specificity 76% and 71%, Table 1). LMM showed that all A+ thresholds had comparable associations with rate of memory decline to VA (range β ‐0.39 − ‐0.48). With increasing quantile‐levels, memory slopes gradually became steeper for both BP ND and SUVr. The predefined grey zone (BP ND 0.18‐0.27, SUVr 1.27‐1.42) was significantly associated with memory decline for both BP ND (β ‐0.29(SE 0.14)) and SUVr (β ‐0.43 (SE 0.14)). Conclusion We showed that amyloid positivity thresholds for BP ND and SUVr are similar to visual assessment in their association with memory decline. Furthermore, the association between A+ and memory decline is not only driven by individuals with the highest amyloid values, but individuals with grey zone amyloid burden are also at risk of steeper memory decline. Therefore, in case a binary classification is required, we suggest using a relatively low threshold, e.g. BP ND 0.18, which includes the grey zone.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S5
    DOI: 10.1002/alz.045210
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 2
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    Subjective cognitive decline and self‐reported sleep at a memory clinic: The SCIENCe project
    Wiley ; 2021
    In:  Alzheimer's & Dementia Vol. 17, No. S10 ( 2021-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 17, No. S10 ( 2021-12)
    Abstract: sleep problems have been associated with Alzheimer’s disease (AD) pathology and they have been suggested to occur early in the disease process. Sleep problems have also been associated with subjective cognitive decline (SCD), although in many subjects with SCD, no AD biomarker evidence is found for the experienced cognitive decline. Our aim was to investigate whether frequency and type of sleep problems in memory clinic patients with SCD are associated with cognition, mental health, MRI measures, and AD CSF biomarkers. Method 308 subjects (65±8yrs, 44% female, MMSE 29±1) from the Subjective Cognitive Impairment Cohort (SCIENCe) project with available information on sleep were included. Sleep was evaluated by the Berlin Questionnaire (3 categories; ≥2 high risk sleep apnea) and Pittsburgh Sleep Quality Index (range 0‐21; ≥5 poor sleep quality). All underwent a standardized memory clinic work‐up. Subjects were classified as having sleep problems when ≥1 sleep questionnaire was above the cut‐off. Sociodemographics, cognitive performance (attention, memory, language, and executive functioning), depressive symptoms, anxiety, self‐reported cognitive decline (Cognitive Change Index; CCI), medial temporal lobe atrophy, global cortical atrophy, white matter hyperintensities, and CSF levels of Aβ42, t‐tau, p‐tau were compared between subjects with and without sleep problems. Result 198/308 (64%) subjects reported sleep problems, based on 107 (35%) sleep apnea and 162 (53%) poor sleep quality. Subjects with sleep problems tended to be younger (63.8±8.1 vs 65.7±8.5), more often female (47% vs 39%) and more often APOE ε4 carrier (40% vs 28%), but these differences did not reach statistical significance (all p 〉 .05, Table 1). They reported more depressive symptoms (CES‐D median(IQR): 10(5‐16) vs 4(2‐7)), anxiety (HADS‐A: 5(2‐10) vs 2(0.25‐4)) and cognitive decline (CCI: 43(31‐56) vs 35(25‐47)), all p ≤.001. Sociodemographics, cognitive performance, MRI measures and AD CSF biomarker levels did not differ between groups. Conclusion sleep problems are common in subjects with SCD and are associated with higher levels of anxiety, depressive symptoms and self‐reported cognitive decline, but not AD biomarkers. Our results suggest that poor sleep quality and hygiene are a potentially reversible cause of the subjective experience of cognitive decline and potential leads for treatment in many subjects with SCD.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v17.S10
    DOI: 10.1002/alz.055412
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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  • 3
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    Polygenic risk score for Alzheimer’s disease is related to amyloid positivity in subjective cognitive decline: The SCIENCe project : Neuroimaging: Imaging genetics
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S4 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S4 ( 2020-12)
    Abstract: The majority of individuals with subjective cognitive decline (SCD) is worried well, but in some the subjective experience of cognitive decline herald’s incipient neurodegenerative disease. Understanding the determinants of disease in SCD is important to separate wheat from chaff. Here we studied APOE and a polygenic risk score for Alzheimer’s disease (AD) in a cohort of SCD that was classified according to the ATN‐framework. Method We classified 542 participants with SCD (59.2±8.7 years, 38.9%Female, MMSE 28.3±1.5) from the Amsterdam Dementia Cohort and SCIENCe project according to the ATN‐framework, as determined by amyloid PET or CSF Abeta(A), CSF p‐tau(T) and MRI‐based medial temporal lobe atrophy(N). We reduced the number of categories to three: controls (A‐T‐N‐ or normal AD biomarkers, N=310(57%)), non‐AD pathologic change (A‐T‐N+, A‐T+N‐, A‐T+N+, N=142 (26%)) and the Alzheimer’s continuum (A+T‐N‐, A+T‐N+, A+T+N‐, A+T+N+, N=90(17%)). We determined APOE ɛ4 and 39 other genetic variants that were associated in previous studies with AD using array genotyping or imputation. A weighted AD polygenic risk score (AD‐PRS) was calculated based on 39 variants (excluding APOE ɛ4). Logistic regression models were fitted for the associations between AD‐PRS and APOE ɛ4 with Alzheimer’s continuum and non‐AD pathological changes. For 324 participants follow‐up for dementia was available (3.1±2.5 year) and progression could be studied. Cox proportional hazard models were used to analyse progression to all‐cause dementia (N=36, 6.6%) and AD‐dementia (N=22, 3.6%). Associations were corrected for 5 ancestry principal components. Result The APOE ɛ4 genotype was associated with Alzheimer’s continuum (OR=3.6, 95%CI 2.4‐5.3, P =3.0×10 ‐10 ) as well as non‐AD pathologic changes (OR=1.5, 95%CI 1.1‐2.2, P =1.6×10 ‐2 ). The AD‐PRS was associated with Alzheimer’s continuum (OR per 1‐SD =1.4, 95%CI 1.1‐1.8, P =3.5×10 ‐3 ), but not with non‐AD pathologic changes (OR=1.1, 95%CI 0.9‐1.3, P =0.64). In the progression analysis: APOE ɛ4 was associated with all‐cause dementia (HR=1.7, 95%CI 1.1‐2.7, P =2.3×10 ‐2 ) as well as AD‐dementia (HR=2.3, 95%CI 1.3‐4.2, P =4.5×10 ‐3 ). The AD‐PRS was not associated with progression to all‐cause dementia (HR=0.9, P =0.4) or AD‐dementia (HR=1.4, P =0.13). Conclusion In individuals with SCD APOE ɛ4 and an AD‐PRS are associated with the presence of amyloid biomarkers (Alzheimer’s continuum), showing that genetic factors can identify individuals at risk in individuals that are cognitively normal.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S4
    DOI: 10.1002/alz.042116
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 4
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    Serum glial fibrillary acidic protein and neurofilament light as prognostic biomarkers for clinical progression in subjective cognitive decline: The SCIENCe project : Biomarkers (non‐neuroimaging): Multimodal biomarker studies in cognitively unimpaired cohorts
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S5 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S5 ( 2020-12)
    Abstract: Blood‐based biomarkers might be easy‐to‐use tools for predicting future decline to dementia in cognitively normal individuals presenting at memory clinics (i.e. subjective cognitive decline; SCD). We previously found that glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) relate to neurodegenerative disease processes ( Verberk, AAIC 2019 ). In this study we aimed to assess the prognostic value, by investigating the relation between baseline serum GFAP and NfL and cognitive decline in individuals with SCD. Method We included 303 individuals with SCD from the Amsterdam Dementia Cohort and SCIENCe project (age 61±9 years, 42% females, MMSE 28±2), who were followed annually for re‐evaluation of diagnosis and cognitive performance on a standardized neuropsychological test battery covering global cognition and the main cognitive domains (average follow‐up: 3.5 ± 2.6 years, median number visits: 3 (range 2‐12), total evaluations: 1014). Baseline serum NfL and GFAP were measured using Simoa, and Z‐transformed levels were associated with incident dementia in age and sex‐adjusted COX regression models, and with longitudinal neuropsychological test performance in age, sex and education‐adjusted linear mixed models. Result Upon follow‐up, 27(9%) individuals developed dementia (18 Alzheimer’s, 9 non‐Alzheimer’s). High baseline GFAP was associated with increased risk of progression to dementia (HR=3.5 (95%CI: 2.2–5.7); Figure 1A), as was high baseline NfL (HR=1.8 (95%CI: 1.2–2.8); Figure 1B). When simultaneously entering both serum markers, only GFAP remained independently associated with risk of dementia (HR=3.2 (1.9–5.4); NfL: HR=1.3 (0.8–2.0)). Additionally entering plasma amyloid showed that both GFAP (HR=2.6 (1.4–4.8) and amyloid (HR=2.4 (1.2–4.5)) independently associated with risk of dementia. Investigating trajectories of cognitive decline, we found that higher baseline GFAP was associated with a steeper rate of decline on tests for global cognition, memory, attention and executive functioning (range standardized betas: ‐0.03–‐0.17, all: p 〈 0.05 FDR ), but not language, whereas for NfL, none of the associations were significant after multiple testing correction (Table 1). Conclusion Our results suggest that especially GFAP is a putative prognostic blood‐based biomarker for identifying individuals with SCD at‐risk for future clinical disease progression. Serum NfL proves to be less useful as a prognostic marker in these earliest disease stages.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S5
    DOI: 10.1002/alz.044783
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 5
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    Association of CSF, Plasma, and Imaging Markers of Neurodegeneration With Clinical Progression in People With Subjective Cognitive Decline
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Neurology Vol. 98, No. 13 ( 2022-03-29), p. e1315-e1326
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 13 ( 2022-03-29), p. e1315-e1326
    Abstract: Multiple biomarkers have been suggested to measure neurodegeneration (N) in the AT(N) framework, leading to inconsistencies between studies. We investigated the association of 5 N biomarkers with clinical progression and cognitive decline in individuals with subjective cognitive decline (SCD). Methods We included individuals with SCD from the Amsterdam Dementia Cohort and SCIENCe project, a longitudinal cohort study (follow-up 4±3 years). We used the following N biomarkers: CSF total tau (t-tau), medial temporal atrophy visual rating on MRI, hippocampal volume (HV), serum neurofilament light (NfL), and serum glial fibrillary acidic protein (GFAP). We determined correlations between biomarkers. We assessed associations between N biomarkers and clinical progression to mild cognitive impairment or dementia (Cox regression) and Mini-Mental State Examination (MMSE) over time (linear mixed models). Models included age, sex, CSF β-amyloid (Aβ) (A), and CSF p-tau (T) as covariates, in addition to the N biomarker. Result We included 401 individuals (61±9 years, 42% female, MMSE 28 ± 2, vascular comorbidities 8%–19%). N biomarkers were modestly to moderately correlated (range r −0.28 – 0.58). Serum NfL and GFAP correlated most strongly ( r 0.58, p 〈 0.01). T-tau was strongly correlated with p-tau ( r 0.89, p 〈 0.01), although these biomarkers supposedly represent separate biomarker groups. All N biomarkers individually predicted clinical progression, but only HV, NfL, and GFAP added predictive value beyond Aβ and p-tau (hazard ratio 1.52 [95% CI 1.11–2.09]; 1.51 [1.05–2.17] ; 1.50 [1.04–2.15]). T-tau, HV, and GFAP individually predicted MMSE slope (range β −0.17 to −0.11, p 〈 0.05), but only HV remained associated beyond Aβ and p-tau (β −0.13 [SE 0.04]; p 〈 0.05). Discussion In cognitively unimpaired older adults, correlations between different N biomarkers were only moderate, indicating they reflect different aspects of neurodegeneration and should not be used interchangeably. T-tau was strongly associated with p-tau (T), which makes it less desirable to use as a measure for N. HV, NfL, and GFAP predicted clinical progression beyond A and T. Our results do not allow to choose one most suitable biomarker for N, but illustrate the added prognostic value of N beyond A and T. Classification of Evidence This study provides Class II evidence that HV, NfL, and GFAP predicted clinical progression beyond A and T in individuals with SCD.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000200035
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
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  • 6
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    Longitudinal change in ATN biomarkers in cognitively normal individuals
    Springer Science and Business Media LLC ; 2022
    In:  Alzheimer's Research & Therapy Vol. 14, No. 1 ( 2022-09-03)
    Details
    In: Alzheimer's Research & Therapy, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2022-09-03)
    Abstract: Biomarkers for amyloid, tau, and neurodegeneration (ATN) have predictive value for clinical progression, but it is not clear how individuals move through these stages. We examined changes in ATN profiles over time, and investigated determinants of change in A status, in a sample of cognitively normal individuals presenting with subjective cognitive decline (SCD). Methods We included 92 individuals with SCD from the SCIENCe project with [ 18 F]florbetapir PET (A) available at two time points (65 ± 8y, 42% female, MMSE 29 ± 1, follow-up 2.5 ± 0.7y). We additionally used [ 18 F]flortaucipir PET for T and medial temporal atrophy score on MRI for N. Thirty-nine individuals had complete biomarker data at baseline and follow-up, enabling the construction of ATN profiles at two time points. All underwent extensive neuropsychological assessments (follow-up time 4.9 ± 2.8y, median number of visits n  = 4). We investigated changes in biomarker status and ATN profiles over time. We assessed which factors predisposed for a change from A− to A+ using logistic regression. We additionally used linear mixed models to assess change from A− to A+, compared to the group that remained A− at follow-up, as predictor for cognitive decline. Results At baseline, 62% had normal AD biomarkers (A−T−N− n  = 24), 5% had non-AD pathologic change (A−T−N+ n  = 2,) and 33% fell within the Alzheimer’s continuum (A+T−N− n  = 9, A+T+N− n  = 3, A+T+N+ n  = 1). Seventeen subjects (44%) changed to another ATN profile over time. Only 6/17 followed the Alzheimer’s disease sequence of A → T → N, while 11/17 followed a different order (e.g., reverted back to negative biomarker status). APOE ε4 carriership inferred an increased risk of changing from A− to A+ (OR 5.2 (95% CI 1.2–22.8)). Individuals who changed from A− to A+, showed subtly steeper decline on Stroop I ( β − 0.03 (SE 0.01)) and Stroop III (− 0.03 (0.01)), compared to individuals who remained A−. Conclusion We observed considerable variability in the order of ATN biomarkers becoming abnormal. Individuals who became A+ at follow-up showed subtle decline on tests for attention and executive functioning, confirming clinical relevance of amyloid positivity.
    Type of Medium: Online Resource
    ISSN: 1758-9193
    URL: Article
    DOI: 10.1186/s13195-022-01069-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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  • 7
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    Amyloid pathology, but not vascular pathology, is associated with risk of incident dementia in non‐demented memory clinic participants : Neuroimaging: Neuroimaging predictors of cognitive decline
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S5 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S5 ( 2020-12)
    Abstract: Cerebral accumulation of amyloid contributes to cognitive decline and progression to dementia. Also vascular pathologies have been suggested to contribute to dementia. We investigated the putative additional effects of vascular and amyloid pathology in patients with subjective cognitive decline (SCD) and mild cognitive impairment (MCI). Method We included patients with SCD (n=294; age 62±6, 40%F, MMSE 27±2) or MCI (n=266; age 66±7, 34%F, MMSE 27±2) from the Amsterdam Dementia Cohort (ADC), with available baseline amyloid status (by CSF or PET), available MRI and longitudinal follow‐up ( 〉 1 year). Patients were defined as amyloid positive (A+) when either CSF Aβ 1‐42 or amyloid‐PET scan was abnormal. Vascular positive (V+) was defined as having at least one abnormal vascular MRI marker (Fazekas score 2 or 3, microbleeds ≥1 or lacunar infarcts ≥1). We used Cox proportional hazard models to analyze progression to dementia with sex and age as covariates, firstly analyzing A+ and V+ separately, followed by both simultaneously. In addition, we analyzed the effect of each vascular component separately. All analyses were stratified for baseline clinical diagnosis (SCD, MCI). Result At baseline 59 (20%) SCD patients were A+ and 75 (26%) V+, 142 (54%) MCI participants A+ and 124 (47%) V+. At follow‐up (3.0 ± 1.9yrs), 21 (7%) SCD and 92 (35%) MCI developed dementia (Table 1). In both SCD and MCI, amyloid pathology was associated with increased risk of dementia (SCD: HR[95%CI]=4.8[2.5‐9.0] ; MCI: 1.7[1.2‐2.5]), while the presence of vascular pathology was not (SCD1.5[0.8‐2.7] ; MCI: 0.9[0.6‐1.2]). When we entered both determinants simultaneously in one model, associations remained largely similar. There was no interaction between amyloid and vascular pathology (SCD: HR=0.7, CI95%=0.2‐2.6; MCI: HR=0.89, CI95%=0.4‐1.78). When analyzing the three vascular components separately, we found a trend association of microbleeds with incident dementia in SCD, but not in MCI (SCD: HR[95%CI] =2.3[0.96‐5.4]; MCI: 0.8 [0.5‐1.3] ). Conclusion In this memory clinic cohort of patients with SCD and MCI, we found that – although amyloid pathology and vascular pathology were equally prevalent – only amyloid pathology was associated with incident dementia.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S5
    DOI: 10.1002/alz.045196
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 8
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    Subjective cognitive decline and clinical progression in the memory clinic: The value of longitudinal self‐ and informant‐report in the SCIENCe project
    Wiley ; 2022
    In:  Alzheimer's & Dementia Vol. 18, No. S7 ( 2022-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 18, No. S7 ( 2022-12)
    Abstract: Among memory clinic patients who report the experience of subjective cognitive decline (SCD), only a small percentage are in a preclinical stage of Alzheimer’s disease (AD). We aimed to investigate how longitudinal self‐ and informant report of SCD relate to AD biomarkers and clinical progression. Method We followed 409 individuals with SCD (63±9 years, n = 180 (44%) female, MMSE 27.7±4.6) from the SCIENCe project over time, with yearly visits ( n observations = 1,436, 2.7±1.7 years follow‐up). At baseline, amyloid was measured in cerebrospinal fluid or using amyloid positron emission tomography scans ( n = 328, 80%) and dichotomized into positive ( n = 100, 30%) or negative for AD ( n = 228). We assessed degree of subjective complaints using both self and informant‐reported Cognitive Change Index (CCI). Using linear mixed models with random intercepts and slopes, CCI‐self and CCI‐informant were related to time and amyloid. In Cox regressions, we investigated the association between dichotomized baseline CCI and clinical progression to MCI or dementia (progressors n = 25). Models were adjusted for age, sex and education. Result At baseline, CCI‐self (intercept [95% confidence interval (95%CI)] = 45.20 [33.94, 56.43] ) were higher than CCI‐informant scores (intercept [95%CI] = 45.39 [32.59, 58.15] ). CCI‐informant scores of amyloid positive participants increased over time (estimate [95%CI] = 1.8 [0.5, 3.1] ) whereas they did not in amyloid negative participants (estimate [95%CI] = ‐0.6 [‐1.3, 0.2] ; Table 1). CCI‐self scores decreased in amyloid negative, but not in amyloid positive participants, although the rates of change did not differ significantly from each other (amyloid‐time interaction = 1.0, 95% confidence interval (95%CI) = [‐0.3, 2.2]; Figure 1, Table 1). High baseline CCI‐informant (hazard ratio (HR) = 4.8, 95%CI = [1.1, 21.4] ), but not CCI‐self (HR = 5.3, 95%CI = [0.7, 40.5]), was associated with a higher risk of clinical progression. Conclusion Our results highlight the value of longitudinal self and informant‐report in the measurement of SCD. We found an effect of amyloid positivity on change in informant‐reported CCI and informant report also predicted clinical progression. Rates of change in self‐reported CCI scores did not differ significantly between amyloid positive and negative participants, which may hint at a waning awareness among those individuals with SCD due to AD pathology. Our work implies that informant‐report may be especially valuable in longitudinal studies.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v18.S7
    DOI: 10.1002/alz.061349
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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    ATN classification in dementia with Lewy bodies: Association with clinical profile, cognitive decline and survival
    Wiley ; 2021
    In:  Alzheimer's & Dementia Vol. 17, No. S4 ( 2021-12)
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    In: Alzheimer's & Dementia, Wiley, Vol. 17, No. S4 ( 2021-12)
    Abstract: The ATN framework has been developed to characterize biological processes within the Alzheimer’s disease (AD) continuum. Since AD pathology often coincides with dementia with Lewy Bodies (DLB), we aimed to examine the distribution of ATN profiles in DLB and associate ATN‐profiles in DLB to prognosis. Method We included 192 DLB patients from the Amsterdam Dementia Cohort (68±7yrs, 19%F, MMSE: 24±3, DAT‐SPECT abnormal: 104/114). Patients were classified according to the ATN framework, using CSF Aβ 1‐42 (A), CSF p‐tau (T) and medial temporal atrophy scores (N). Categories were compared on presence of clinical symptoms and demographics. To yield sufficient power for longitudinal analyses, the eight profiles were combined into four categories: normal AD biomarkers (A‐T‐N‐, reference), non‐AD pathologic change (A–T–N+/A–T+N–/A–T+N+), amyloid‐only (A+T‐N‐) and amyloid‐plus (A+T–N+/A+T+N–/A+T+N+). We used linear mixed models to analyze decline in MMSE (follow‐up 3±2yrs for n=137). We assessed differences in mortality using Cox proportional‐hazards models. Result Fifty (26%) DLB patients had normal AD biomarkers (A‐T‐N‐), 36 (19%) had non‐AD pathologic change (A‐T+N‐: 10%/A‐T‐N+: 6%/A‐T+N+: 3%) and 106 (55%) were classified within the AD‐continuum (A+T‐N‐: 20%/A+T+N‐: 16%/A+T‐N+: 10%/A+T+N+: 9%)(figure 1). A+T+N+ patients were older and less often had RBD symptoms. Compared to patients with normal AD biomarkers, those with amyloid‐only had steeper decline in MMSE (β±SE=‐0.82±0.28, p =0.005), while amyloid‐plus was associated to higher mortality rate (HR: 1.85[1.09‐3.13]). Cognitive decline and mortality did not differ between non‐AD pathologic change and normal AD biomarkers (figure 2‐3). Conclusion In our DLB cohort, we found clinically relevant associations between ATN categories and disease manifestation. Patients within the AD‐continuum had steeper cognitive decline (especially amyloid‐only) and shorter survival (amyloid‐plus). Individuals with non‐AD pathologic change did not differ from those with normal AD biomarkers in clinical presentation, decline or survival. Implementing the ATN framework within DLB patients could aid in subtyping patients based on underlying biological processes and provide targets for future treatment strategies, e.g. AD modifying treatment.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v17.S4
    DOI: 10.1002/alz.052056
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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    Subjective cognitive decline and self‐reported sleep problems: The SCIENCe project
    Wiley ; 2022
    In:  Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring Vol. 14, No. 1 ( 2022-01)
    Details
    In: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, Wiley, Vol. 14, No. 1 ( 2022-01)
    Abstract: We aim to investigate the frequency and type of sleep problems in memory clinic patients with subjective cognitive decline (SCD) and their association with cognition, mental health, brain magnetic resonance imaging (MRI), and cerebrospinal fluid (CSF) biomarkers. Three hundred eight subjects (65 ± 8 years, 44% female) were selected from the Subjective Cognitive Impairment Cohort (SCIENCe) project. All subjects answered two sleep questionnaires, Berlin Questionnaire (sleep apnea) and Pittsburgh Sleep Quality Index (sleep quality) and underwent a standardized memory clinic work‐up. One hundred ninety‐eight (64%) subjects reported sleep problems, based on 107 (35%) positive screenings on sleep apnea and 162 (53%) on poor sleep quality. Subjects with sleep problems reported more severe depressive symptoms, more anxiety, and more severe SCD. Cognitive tests, MRI, and CSF biomarkers did not differ between groups. Our results suggest that improvement of sleep quality and behaviors are potential leads for treatment in many subjects with SCD to relieve the experienced cognitive complaints.
    Type of Medium: Online Resource
    ISSN: 2352-8729 , 2352-8729
    URL: Issue
    URL: Article
    DOI: 10.1002/dad2.v14.1
    DOI: 10.1002/dad2.12287
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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