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  • 1
    Online Resource
    Online Resource
    Insulin-like growth factor binding protein-2 in at-risk adults and autopsy-confirmed Alzheimer brains
    Oxford University Press (OUP) ; 2024
    In:  Brain Vol. 147, No. 5 ( 2024-05-03), p. 1680-1695
    Details
    In: Brain, Oxford University Press (OUP), Vol. 147, No. 5 ( 2024-05-03), p. 1680-1695
    Abstract: Insulin, insulin-like growth factors (IGF) and their receptors are highly expressed in the adult hippocampus. Thus, disturbances in the insulin-IGF signalling pathway may account for the selective vulnerability of the hippocampus to nascent Alzheimer's disease (AD) pathology. In the present study, we examined the predominant IGF-binding protein in the CSF, IGFBP2. CSF was collected from 109 asymptomatic members of the parental history-positive PREVENT-AD cohort. CSF levels of IGFBP2, core AD and synaptic biomarkers were measured using proximity extension assay, ELISA and mass spectrometry. Cortical amyloid-beta (Aβ) and tau deposition were examined using 18F-NAV4694 and flortaucipir. Cognitive assessments were performed during up to 8 years of follow-up, using the Repeatable Battery for the Assessment of Neuropsychological Status. T1-weighted structural MRI scans were acquired, and neuroimaging analyses were performed on pre-specified temporal and parietal brain regions. Next, in an independent cohort, we allocated 241 dementia-free ADNI-1 participants into four stages of AD progression based on the biomarkers CSF Aβ42 and total-tau (t-tau). In this analysis, differences in CSF and plasma IGFBP2 levels were examined across the pathological stages. Finally, IGFBP2 mRNA and protein levels were examined in the frontal cortex of 55 autopsy-confirmed AD and 31 control brains from the Quebec Founder Population (QFP) cohort, a unique population isolated from Eastern Canada. CSF IGFBP2 progressively increased over 5 years in asymptomatic PREVENT-AD participants. Baseline CSF IGFBP2 was positively correlated with CSF AD biomarkers and synaptic biomarkers, and negatively correlated with longitudinal changes in delayed memory (P = 0.024) and visuospatial abilities (P = 0.019). CSF IGFBP2 was negatively correlated at a trend-level with entorhinal cortex volume (P = 0.082) and cortical thickness in the piriform (P = 0.039), inferior temporal (P = 0.008), middle temporal (P = 0.014) and precuneus (P = 0.033) regions. In ADNI-1, CSF (P = 0.009) and plasma (P = 0.001) IGFBP2 were significantly elevated in Stage 2 [CSF Aβ(+)/t-tau(+)]. In survival analyses in ADNI-1, elevated plasma IGFBP2 was associated with a greater rate of AD conversion (hazard ratio = 1.62, P = 0.021). In the QFP cohort, IGFBP2 mRNA was reduced (P = 0.049); however, IGFBP2 protein levels did not differ in the frontal cortex of autopsy-confirmed AD brains (P = 0.462). Nascent AD pathology may induce an upregulation in IGFBP2 in asymptomatic individuals. CSF and plasma IGFBP2 may be valuable markers for identifying CSF Aβ(+)/t-tau(+) individuals and those with a greater risk of AD conversion.
    Type of Medium: Online Resource
    ISSN: 0006-8950 , 1460-2156
    URL: Article
    DOI: 10.1093/brain/awad398
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2024
    detail.hit.zdb_id: 1474117-9
    detail.hit.zdb_id: 80072-7
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Determinants of cognitive and brain resilience to tau pathology: a longitudinal analysis
    Oxford University Press (OUP) ; 2023
    In:  Brain Vol. 146, No. 9 ( 2023-09-01), p. 3719-3734
    Details
    In: Brain, Oxford University Press (OUP), Vol. 146, No. 9 ( 2023-09-01), p. 3719-3734
    Abstract: Mechanisms of resilience against tau pathology in individuals across the Alzheimer’s disease spectrum are insufficiently understood. Longitudinal data are necessary to reveal which factors relate to preserved cognition (i.e. cognitive resilience) and brain structure (i.e. brain resilience) despite abundant tau pathology, and to clarify whether these associations are cross-sectional or longitudinal. We used a longitudinal study design to investigate the role of several demographic, biological and brain structural factors in yielding cognitive and brain resilience to tau pathology as measured with PET. In this multicentre study, we included 366 amyloid-β-positive individuals with mild cognitive impairment or Alzheimer’s disease dementia with baseline 18F-flortaucipir-PET and longitudinal cognitive assessments. A subset (n = 200) additionally underwent longitudinal structural MRI. We used linear mixed-effects models with global cognition and cortical thickness as dependent variables to investigate determinants of cognitive resilience and brain resilience, respectively. Models assessed whether age, sex, years of education, APOE-ε4 status, intracranial volume (and cortical thickness for cognitive resilience models) modified the association of tau pathology with cognitive decline or cortical thinning. We found that the association between higher baseline tau-PET levels (quantified in a temporal meta-region of interest) and rate of cognitive decline (measured with repeated Mini-Mental State Examination) was adversely modified by older age (Stβinteraction = −0.062, P = 0.032), higher education level (Stβinteraction = −0.072, P = 0.011) and higher intracranial volume (Stβinteraction = −0.07, P = 0.016). Younger age, higher education and greater cortical thickness were associated with better cognitive performance at baseline. Greater cortical thickness was furthermore associated with slower cognitive decline independent of tau burden. Higher education also modified the negative impact of tau-PET on cortical thinning, while older age was associated with higher baseline cortical thickness and slower rate of cortical thinning independent of tau. Our analyses revealed no (cross-sectional or longitudinal) associations for sex and APOE-ε4 status on cognition and cortical thickness. In this longitudinal study of clinically impaired individuals with underlying Alzheimer’s disease neuropathological changes, we identified education as the most robust determinant of both cognitive and brain resilience against tau pathology. The observed interaction with tau burden on cognitive decline suggests that education may be protective against cognitive decline and brain atrophy at lower levels of tau pathology, with a potential depletion of resilience resources with advancing pathology. Finally, we did not find major contributions of sex to brain nor cognitive resilience, suggesting that previous links between sex and resilience might be mainly driven by cross-sectional differences.
    Type of Medium: Online Resource
    ISSN: 0006-8950 , 1460-2156
    URL: Article
    DOI: 10.1093/brain/awad100
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1474117-9
    detail.hit.zdb_id: 80072-7
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Towards cascading genetic risk in Alzheimer’s disease
    Oxford University Press (OUP) ; 2024
    In:  Brain Vol. 147, No. 8 ( 2024-08-01), p. 2680-2690
    Details
    In: Brain, Oxford University Press (OUP), Vol. 147, No. 8 ( 2024-08-01), p. 2680-2690
    Abstract: Alzheimer’s disease typically progresses in stages, which have been defined by the presence of disease-specific biomarkers: amyloid (A), tau (T) and neurodegeneration (N). This progression of biomarkers has been condensed into the ATN framework, in which each of the biomarkers can be either positive (+) or negative (−). Over the past decades, genome-wide association studies have implicated ∼90 different loci involved with the development of late-onset Alzheimer’s disease. Here, we investigate whether genetic risk for Alzheimer’s disease contributes equally to the progression in different disease stages or whether it exhibits a stage-dependent effect. Amyloid (A) and tau (T) status was defined using a combination of available PET and CSF biomarkers in the Alzheimer’s Disease Neuroimaging Initiative cohort. In 312 participants with biomarker-confirmed A−T− status, we used Cox proportional hazards models to estimate the contribution of APOE and polygenic risk scores (beyond APOE) to convert to A+T− status (65 conversions). Furthermore, we repeated the analysis in 290 participants with A+T− status and investigated the genetic contribution to conversion to A+T+ (45 conversions). Both survival analyses were adjusted for age, sex and years of education. For progression from A−T− to A+T−, APOE-e4 burden showed a significant effect [hazard ratio (HR) = 2.88; 95% confidence interval (CI): 1.70–4.89; P & lt; 0.001], whereas polygenic risk did not (HR = 1.09; 95% CI: 0.84–1.42; P = 0.53). Conversely, for the transition from A+T− to A+T+, the contribution of APOE-e4 burden was reduced (HR = 1.62; 95% CI: 1.05–2.51; P = 0.031), whereas the polygenic risk showed an increased contribution (HR = 1.73; 95% CI: 1.27–2.36; P & lt; 0.001). The marginal APOE effect was driven by e4 homozygotes (HR = 2.58; 95% CI: 1.05–6.35; P = 0.039) as opposed to e4 heterozygotes (HR = 1.74; 95% CI: 0.87–3.49; P = 0.12). The genetic risk for late-onset Alzheimer’s disease unfolds in a disease stage-dependent fashion. A better understanding of the interplay between disease stage and genetic risk can lead to a more mechanistic understanding of the transition between ATN stages and a better understanding of the molecular processes leading to Alzheimer’s disease, in addition to opening therapeutic windows for targeted interventions.
    Type of Medium: Online Resource
    ISSN: 0006-8950 , 1460-2156
    URL: Article
    DOI: 10.1093/brain/awae176
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2024
    detail.hit.zdb_id: 1474117-9
    detail.hit.zdb_id: 80072-7
    SSG: 12
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Interpretable discriminant analysis for functional data supported on random nonlinear domains with an application to Alzheimer’s disease
    Oxford University Press (OUP) ; 2024
    In:  Journal of the Royal Statistical Society Series B: Statistical Methodology ( 2024-03-22)
    Details
    In: Journal of the Royal Statistical Society Series B: Statistical Methodology, Oxford University Press (OUP), ( 2024-03-22)
    Abstract: We introduce a novel framework for the classification of functional data supported on nonlinear, and possibly random, manifold domains. The motivating application is the identification of subjects with Alzheimer’s disease from their cortical surface geometry and associated cortical thickness map. The proposed model is based upon a reformulation of the classification problem as a regularized multivariate functional linear regression model. This allows us to adopt a direct approach to the estimation of the most discriminant direction while controlling for its complexity with appropriate differential regularization. Our approach does not require prior estimation of the covariance structure of the functional predictors, which is computationally prohibitive in our application setting. We provide a theoretical analysis of the out-of-sample prediction error of the proposed model and explore the finite sample performance in a simulation setting. We apply the proposed method to a pooled dataset from Alzheimer’s Disease Neuroimaging Initiative and Parkinson’s Progression Markers Initiative. Through this application, we identify discriminant directions that capture both cortical geometric and thickness predictive features of Alzheimer’s disease that are consistent with the existing neuroscience literature.
    Type of Medium: Online Resource
    ISSN: 1369-7412 , 1467-9868
    URL: Article
    DOI: 10.1093/jrsssb/qkae023
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2024
    detail.hit.zdb_id: 204795-0
    detail.hit.zdb_id: 1490719-7
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  • 5
    Online Resource
    Online Resource
    Re-examining the characteristics of pediatric multiple sclerosis in the era of antibody-associated demyelinating syndromes
    Elsevier BV ; 2022
    In:  European Journal of Paediatric Neurology Vol. 41 ( 2022-11), p. 8-18
    Details
    In: European Journal of Paediatric Neurology, Elsevier BV, Vol. 41 ( 2022-11), p. 8-18
    Type of Medium: Online Resource
    ISSN: 1090-3798
    URL: Article
    DOI: 10.1016/j.ejpn.2022.08.006
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1397146-3
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  • 6
    Online Resource
    Online Resource
    Anatomically interpretable deep learning of brain age captures domain-specific cognitive impairment
    Proceedings of the National Academy of Sciences ; 2023
    In:  Proceedings of the National Academy of Sciences Vol. 120, No. 2 ( 2023-01-10)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 120, No. 2 ( 2023-01-10)
    Abstract: The gap between chronological age (CA) and biological brain age, as estimated from magnetic resonance images (MRIs), reflects how individual patterns of neuroanatomic aging deviate from their typical trajectories. MRI-derived brain age (BA) estimates are often obtained using deep learning models that may perform relatively poorly on new data or that lack neuroanatomic interpretability. This study introduces a convolutional neural network (CNN) to estimate BA after training on the MRIs of 4,681 cognitively normal (CN) participants and testing on 1,170 CN participants from an independent sample. BA estimation errors are notably lower than those of previous studies. At both individual and cohort levels, the CNN provides detailed anatomic maps of brain aging patterns that reveal sex dimorphisms and neurocognitive trajectories in adults with mild cognitive impairment (MCI, N  = 351) and Alzheimer’s disease (AD, N  = 359). In individuals with MCI (54% of whom were diagnosed with dementia within 10.9 y from MRI acquisition), BA is significantly better than CA in capturing dementia symptom severity, functional disability, and executive function. Profiles of sex dimorphism and lateralization in brain aging also map onto patterns of neuroanatomic change that reflect cognitive decline. Significant associations between BA and neurocognitive measures suggest that the proposed framework can map, systematically, the relationship between aging-related neuroanatomy changes in CN individuals and in participants with MCI or AD. Early identification of such neuroanatomy changes can help to screen individuals according to their AD risk.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2214634120
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2023
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Seasonal influenza vaccination coverage: a multicenter cross-sectional study among healthcare workers
    Modestum Ltd ; 2020
    In:  Ortadoğu Tıp Dergisi Vol. 12, No. 1 ( 2020-03-01), p. 113-119
    Details
    In: Ortadoğu Tıp Dergisi, Modestum Ltd, Vol. 12, No. 1 ( 2020-03-01), p. 113-119
    Type of Medium: Online Resource
    ISSN: 1309-3630 , 2548-0251
    URL: Article
    DOI: 10.21601/ortadogutipdergisi.658876
    Language: Unknown
    Publisher: Modestum Ltd
    Publication Date: 2020
    detail.hit.zdb_id: 2689102-5
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  • 8
    Online Resource
    Online Resource
    PP-184 Relationship Between Vitamin 12 and Syntax Score
    Elsevier BV ; 2016
    In:  The American Journal of Cardiology Vol. 117 ( 2016-06), p. S108-
    Details
    In: The American Journal of Cardiology, Elsevier BV, Vol. 117 ( 2016-06), p. S108-
    Type of Medium: Online Resource
    ISSN: 0002-9149
    URL: Article
    DOI: 10.1016/j.amjcard.2016.04.275
    RVK:
    XA 18500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 80014-4
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  • 9
    Online Resource
    Online Resource
    Neuroimaging predictors of brain amyloidosis in mild cognitive impairment
    Wiley ; 2013
    In:  Annals of Neurology Vol. 74, No. 2 ( 2013-08), p. 188-198
    Details
    In: Annals of Neurology, Wiley, Vol. 74, No. 2 ( 2013-08), p. 188-198
    Abstract: To identify a neuroimaging signature predictive of brain amyloidosis as a screening tool to identify individuals with mild cognitive impairment (MCI) that are most likely to have high levels of brain amyloidosis or to be amyloid‐free. Methods The prediction model cohort included 62 MCI subjects screened with structural magnetic resonance imaging (MRI) and 11 C‐labeled Pittsburgh compound B positron emission tomography (PET). We identified an anatomical shape variation‐based neuroimaging predictor of brain amyloidosis and defined a structural MRI‐based brain amyloidosis score (sMRI‐BAS). Amyloid beta positivity (Aβ + ) predictive power of sMRI‐BAS was validated on an independent cohort of 153 MCI patients with cerebrospinal fluid Aβ 1–42 biomarker data but no amyloid PET scans. We compared the Aβ + predictive power of sMRI‐BAS to those of apolipoprotein E (ApoE) genotype and hippocampal volume, the 2 most relevant candidate biomarkers for the prediction of brain amyloidosis. Results Anatomical shape variations predictive of brain amyloidosis in MCI embraced a characteristic spatial pattern known for high vulnerability to Alzheimer disease pathology, including the medial temporal lobe, temporal–parietal association cortices, posterior cingulate, precuneus, hippocampus, amygdala, caudate, and fornix/stria terminals. Aβ + prediction performance of sMRI‐BAS and ApoE genotype jointly was significantly better than the performance of each predictor separately (area under the curve [AUC] = 0.88 vs AUC = 0.70 and AUC = 0.81, respectively) with 〉 90% sensitivity and specificity at 20% false‐positive rate and false‐negative rate thresholds. Performance of hippocampal volume as an independent predictor of brain amyloidosis in MCI was only marginally better than random chance (AUC = 0.56). Interpretation As one of the first attempts to use an imaging technique that does not require amyloid‐specific radioligands for identification of individuals with brain amyloidosis, our findings could lead to development of multidisciplinary/multimodality brain amyloidosis biomarkers that are reliable, minimally invasive, and widely available. Ann Neurol 2013;74:188–198
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v74.2
    DOI: 10.1002/ana.23921
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 80362-5
    detail.hit.zdb_id: 2037912-2
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  • 10
    Online Resource
    Online Resource
    Chronic depressive symptomatology and CSF amyloid beta and tau levels in mild cognitive impairment
    Wiley ; 2018
    In:  International Journal of Geriatric Psychiatry Vol. 33, No. 10 ( 2018-10), p. 1305-1311
    Details
    In: International Journal of Geriatric Psychiatry, Wiley, Vol. 33, No. 10 ( 2018-10), p. 1305-1311
    Abstract: To investigate the association between chronic subsyndromal symptoms of depression (SSD), cerebrospinal fluid (CSF) biomarkers, and neuropsychological performance in individuals with mild cognitive impairment (MCI). Methods Participants included 238 older adults diagnosed with MCI from the Alzheimer's Disease Neuroimaging Initiative repository with cognitive and CSF amyloid beta (Aβ 1–42 ), total tau (t‐tau), and phosphorylated tau (p‐tau) data. The Neuropsychiatric Inventory identified individuals with chronic endorsement (SSD group N  = 80) or no endorsement (non‐SSD group N  = 158) of depressive symptoms across timepoints. CSF biomarker and cognitive performance were evaluated with linear regression models adjusting for age, education, gender, APOE genotype, global cognitive status, and SSD group. Results As compared to the non‐SSD group, the SSD group displayed lower CSF Aβ 1–42 levels (β = −24.293, S.E. = 6.345, P   〈  0.001). No group differences were observed for CSF t‐tau ( P  = 0.497) or p‐tau levels ( P  = 0.392). Lower CSF Aβ 1–42 levels were associated with poorer performance on learning (β = 0.041, S.E. = 0.018, P  = 0.021) and memory (β = −0.012, S.E. = 0.005, P  = 0.031) measures, whereas higher CSF t‐tau levels were associated with poorer performance on measures of global cognition (β = 0.022, S.E = 0.008, P  = 0.007) and language (β = −0.010, S.E = 0.004, P  = 0.019). SSD was independently associated with diminished global cognition, learning and memory, language, and executive function performance over and above the effects of CSF biomarkers (all P   〈  0.05). Conclusions MCI participants with SSD displayed diminished CSF Aβ 1–42 levels but did not differ from non‐SSD controls in CSF tau levels. Additionally, CSF biomarkers and SSD independently accounted for variance in cognitive performance, suggesting that these factors may uniquely confer cognitive risk in MCI.
    Type of Medium: Online Resource
    ISSN: 0885-6230 , 1099-1166
    URL: Issue
    URL: Article
    DOI: 10.1002/gps.v33.10
    DOI: 10.1002/gps.4926
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 806736-3
    detail.hit.zdb_id: 1500455-7
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