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  • 1
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    Associations between peripheral hearing ability at age 70, brain atrophy and cognitive decline in adults born in the same week of 1946
    Wiley ; 2023
    In:  Alzheimer's & Dementia Vol. 19, No. S8 ( 2023-06)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 19, No. S8 ( 2023-06)
    Abstract: Peripheral hearing impairment has been proposed as a risk factor for dementia. However, the relationship between hearing ability, neurodegeneration and cognitive decline, and the extent to which pathological processes associated with increased risk of specific causes of dementia, such as β‐amyloid and small vessel disease, influence these relationships, is unclear. Method Data were analysed from 287 cognitively normal adults born in the same week of 1946 who underwent pure tone audiometry testing at baseline (mean age = 70.6 years), with cognitive assessment and brain imaging at baseline and at follow‐up on average 2.4 years later. Peripheral hearing impairment was defined as a pure tone average of greater than 25 decibels in the best hearing ear. Rates of change for whole brain, hippocampal and ventricle volume were estimated from structural MRI using the Boundary Shift Integral. Cognition was assessed using the Pre‐clinical Alzheimer’s Cognitive Composite. Regression models were performed to evaluate how baseline hearing impairment associated with subsequent brain atrophy and cognitive decline after adjustment for a range of variables including baseline β‐amyloid deposition (assessed using florbetapir‐PET) and baseline small vessel disease burden (estimated using white matter hyperintensity volume). Results 111 out of 287 participants were defined as having peripheral hearing impairment. Hearing impaired individuals demonstrated faster rates of whole brain atrophy (p = 0.031 – figure/table 1) compared with those with normal hearing. Peripheral hearing impairment did not predict change in PACC performance, but there was evidence of an interaction between hearing impairment and whole brain atrophy rates in terms of effect on change in PACC performance. Specifically, faster rates of whole brain atrophy predicted greater cognitive decline in participants with hearing impairment (p = 0.004), whilst there was no evidence of an association between cognitive change and atrophy in participants with preserved hearing (figure/table 2). There was no evidence that β‐amyloid deposition or white matter hyperintensity volume modified these relationships. Conclusion We present evidence of associations between peripheral hearing ability at age 70, brain atrophy and cognitive decline independent of β‐amyloid and small vessel disease, suggesting hearing may associate with brain health via mechanisms distinct from those typically implicated in pre‐clinical Alzheimer’s disease and vascular cognitive impairment.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v19.S8
    DOI: 10.1002/alz.059498
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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  • 2
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    Lifetime cigarette smoking and later‐life brain health: The population‐based 1946 British Birth Cohort : Public health: ADRD risk and protective factors: Brain changes and mechanisms
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S10 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S10 ( 2020-12)
    Abstract: Cigarette smoking is implicated as a risk factor for dementia, but the underlying mechanisms are poorly understood. In a population‐based sample free of dementia, we examine associations between smoking patterns over the life course and imaging markers associated with dementia. Method Dementia‐free participants from Insight 46 (n=458, 49% female, age 69‐71), a sub‐study of the 1946 British Birth Cohort, underwent 18 F‐florbetapir Aβ‐PET and multi‐modal MR imaging including T1, T2, FLAIR and multi‐shell diffusion‐weighted sequences. Information on smoking frequency and cessation (current/former/never) were obtained at multiple timepoints, spanning ages 15‐69 years. Pack‐years were calculated as number of cigarettes smoked/day divided by 20, multiplied by years of smoking. Age and sex adjusted regression analyses examined relationships between smoking metrics and later‐life imaging measures; including Aβ‐PET status, brain, hippocampal and white matter hyperintensity (WMH) volumes, normal appearing white matter (NAWM) fractional anisotropy (FA), mean diffusivity (MD), neurite density index (NDI) and orientation dispersion index (ODI), and Alzheimer’s disease (AD)‐related cortical thickness. Result Increased smoking pack‐years was associated with alterations in NAWM microstructure metrics (lower FA and NDI; higher MD and ODI) and smaller brain and hippocampal volume (Figure 1). There was no significant relationship with Aβ‐PET status (OR=0.99 [95% CI 0.97,1.01]), WMH volume or AD‐related cortical thickness (Figure 1). Unlike current smokers (n=16, 3%), former smokers (n=285, 61%) had comparable NAWM microstructure metrics to those who had never smoked (n=163, 35%). Conclusion In a population‐based sample without dementia or other major neurological problems, increased smoking frequency and duration over 50 years was associated with altered white matter microstructural metrics, and smaller brain and hippocampal volumes. However, there was no evidence that smoking was associated with markers of AD pathology (amyloid‐PET, AD‐related cortical thickness) or cerebral small vessel disease (WMH). Former smokers were comparable to non‐smokers on measures of microstructural metrics, suggesting that smoking‐related microstructural changes may at least partly be reversible. Stopping or reducing smoking may help reduce risks to brain health via microstructural pathways.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S10
    DOI: 10.1002/alz.041111
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 3
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    Longitudinal trajectories of self‐reported subjective cognitive decline in relation to objective cognitive performance in a population‐based cohort
    Wiley ; 2023
    In:  Alzheimer's & Dementia Vol. 19, No. S4 ( 2023-06)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 19, No. S4 ( 2023-06)
    Abstract: Subjective Cognitive Decline (SCD) may represent the onset of cognitive decline before impairment on standard cognitive tests occurs (Jessen et al., 2014). Previous cross‐sectional studies were shown to have limited ability to capture objective differences in cognitive performance between groups with and without SCD (Cacciamani et al., 2017). Understanding the interplay between changes in subjective memory ratings and objective cognitive function over time may have utility in identifying people at risk of dementia. Method 370 cognitively normal (CN) individuals with complete cognitive data ( Table 1 for characteristics) from Insight 46, a longitudinal neuroscience sub‐study of the MRC National Survey for Health and Development (the British 1946 Birth Cohort), underwent cognitive, clinical, and physical assessments, and neuroimaging (combined MRI/18F‐Florbetapir‐PET). SCD was measured using MyCog (Rami et al., 2014) a validated tool, from the SCD‐Questionnaire, where higher scores indicate greater subjective complaints. Linear regression models were used to test whether longitudinal cognitive change as measured using the Preclinical Alzheimer Cognitive Composite (PACC) and a visual short‐term memory binding task were influenced by baseline MyCog and whether there are parallel associations between rates of change in MyCog and longitudinal cognitive change. Covariates were sex, age at baseline visit, childhood cognitive ability, educational attainment, and adult socioeconomic position. Result Baseline MyCog scores did not predict rates of change in PACC or visual short‐term memory binding outcome measures ( Table 2 ). Rates of MyCog change alone did not predict rate of change in PACC, localisation error, total correct number of trials or proportion of misbinding errors ( Table 3 ). However, we observed an interaction effect with baseline amyloid‐b status, whereby greater rates of subjective memory concerns predicted faster rates of decline in the proportion of misbinding errors in amyloid‐b positive participants only ( Table 3; Figure 1 ). Conclusion These findings suggest that higher amyloid‐b burden in CN individuals with subjective memory complaints is associated with faster rates of decline in visual working memory. Corroborating previous reports that feature binding tasks can objectify subtle cognitive deficits found in SCD (Koppara et al., 2015) and serve as a promising tool for identifying people at risk of dementia.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v19.S4
    DOI: 10.1002/alz.067642
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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  • 4
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    Increased variability in reaction time is associated with amyloid beta pathology at age 70
    Wiley ; 2020
    In:  Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring Vol. 12, No. 1 ( 2020-01)
    Details
    In: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, Wiley, Vol. 12, No. 1 ( 2020-01)
    Type of Medium: Online Resource
    ISSN: 2352-8729 , 2352-8729
    URL: Issue
    URL: Article
    DOI: 10.1002/dad2.v12.1
    DOI: 10.1002/dad2.12076
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2832898-X
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  • 5
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    A population‐based study of head injury, cognitive function and pathological markers
    Wiley ; 2021
    In:  Annals of Clinical and Translational Neurology Vol. 8, No. 4 ( 2021-04), p. 842-856
    Details
    In: Annals of Clinical and Translational Neurology, Wiley, Vol. 8, No. 4 ( 2021-04), p. 842-856
    Abstract: To assess associations between head injury (HI) with loss of consciousness (LOC), ageing and markers of later‐life cerebral pathology; and to explore whether those effects may help explain subtle cognitive deficits in dementia‐free individuals. Methods Participants ( n  = 502, age = 69–71) from the 1946 British Birth Cohort underwent cognitive testing (subtests of Preclinical Alzheimer Cognitive Composite), 18 F‐florbetapir A β ‐PET and MR imaging. Measures include A β ‐PET status, brain, hippocampal and white matter hyperintensity (WMH) volumes, normal appearing white matter (NAWM) microstructure, Alzheimer’s disease (AD)‐related cortical thickness, and serum neurofilament light chain (NFL). LOC HI metrics include HI occurring: (i) 〉 15 years prior to the scan (ii) anytime up to age 71. Results Compared to those with no evidence of an LOC HI, only those reporting an LOC HI 〉 15 years prior (16%, n  = 80) performed worse on cognitive tests at age 69–71, taking into account premorbid cognition, particularly on the digit‐symbol substitution test (DSST). Smaller brain volume (BV) and adverse NAWM microstructural integrity explained 30% and 16% of the relationship between HI and DSST, respectively. We found no evidence that LOC HI was associated with A β load, hippocampal volume, WMH volume, AD‐related cortical thickness or NFL (all p   〉  0.01). Interpretation Having a LOC HI aged 50’s and younger was linked with lower later‐life cognitive function at age ~70 than expected. This may reflect a damaging but small impact of HI; explained in part by smaller BV and different microstructure pathways but not via pathology related to AD (amyloid, hippocampal volume, AD cortical thickness) or ongoing neurodegeneration (serum NFL).
    Type of Medium: Online Resource
    ISSN: 2328-9503 , 2328-9503
    URL: Issue
    URL: Article
    DOI: 10.1002/acn3.v8.4
    DOI: 10.1002/acn3.51331
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2740696-9
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  • 6
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    Rates of cortical thinning in Alzheimer’s disease signature regions: pathological influences and cognitive consequences in members of the 1946 British birth cohort
    Wiley ; 2022
    In:  Alzheimer's & Dementia Vol. 18, No. S6 ( 2022-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 18, No. S6 ( 2022-12)
    Abstract: Consistent patterns of reduced cortical thickness (so‐called signature regions) have been identified in early Alzheimer’s disease (AD), including in the pre‐dementia stages, but studies investigating the pathological underpinnings and cognitive consequences of longitudinal changes in these regions have been limited. Method 337 cognitively normal participants (mean [SD] age 70.5 [0.6] years) underwent 18F‐florbetapir amyloid‐ß PET, volumetric MRI, and cognitive assessment as part of Insight 46, a sub‐study of the 1946 British birth cohort (Table 1 for characteristics). Baseline and follow‐up T1‐weighted MRI (mean [SD] interval 2.4 [0.2] years) were processed using Freesurfer’s longitudinal stream (v.7.1.0) and cortical thickness was derived in two AD signatures (Table 2 footnote for details). Linear regression was used to test whether rates of change in AD signature cortical thickness were influenced by baseline amyloid‐ß deposition (positive/negative status or continuous SUVR) or white matter hyperintensity volume (WMHV; a marker of presumed cerebrovascular disease), and whether they were related to longitudinal cognitive change as measured using the Preclinical Alzheimer Cognitive Composite (PACC). Covariates included sex, age at baseline scan, childhood cognition, educational attainment, and socioeconomic position. Interaction terms were added to test whether associations with longitudinal cognitive change differed by baseline amyloid‐ß status. Result Higher baseline WMHV was associated with faster rates of cortical thinning in AD signature regions, but baseline amyloid‐ß status and SUVR were not (Table 2; Figure 1). There were differential effects of rates of change in AD signature cortical thickness by baseline amyloid‐ß status, whereby greater rates of AD signature cortical thinning predicted faster rates of PACC decline in amyloid‐ß positive participants only (Table 3; Figure 2). Conclusion Cortical thinning in AD signature regions may arise via non‐amyloid‐ß pathways in cognitively normal elderly. However, the presence of amyloid‐ß may make individuals more susceptible to the effects of faster rates of cortical thinning in these regions (or vice versa) since these factors interact to influence rates of cognitive decline. These findings provide insight into processes that might underlie progression to dementia in later life and have implications for the utility of AD signature cortical thickness as a biomarker in the preclinical phase of AD.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v18.S6
    DOI: 10.1002/alz.067336
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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  • 7
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    Mid‐life blood pressure and microstructural white matter: Findings from the 1946 British birth cohort : Neuroimaging: Earlier life risk factors and imaging biomarkers
    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: Mid‐life hypertension is an established risk factor for late‐life cognitive impairment. Whilst previous studies demonstrate mid‐life hypertension is associated with larger white matter (WM) hyperintensity volumes, Differences in normal appearing white matter (NAWM) microstructure may provide an earlier indication of WM injury. In a population‐based life‐course study of cognitively healthy individuals, we explored the relationship between blood pressure (BP) over 30 years and NAWM microstructural metrics in later life. Method Participants from Insight 46, a sub‐study of the 1946 British birth cohort, underwent multi‐modal MR imaging including T1, T2, FLAIR and multi‐shell diffusion‐weighted sequences at age 69‐71. Diffusion‐weighted images were processed by automated pipelines, NAWM masks were derived by subtracting the BaMoS‐derived white matter hyperintensity mask from GIF pipeline generated WM mask (eroded by 1 voxel) using FSL. Mean values of microstructural integrity metrics (fractional anisotropy (FA), mean diffusivity (MD), neurite density index (NDI), orientation dispersion index (ODI)) were extracted from T1‐registered diffusion maps using FSL and NODDI toolbox. Individuals with a major brain or neurodegenerative disorder such as dementia, neuroinflammatory condition or stroke were excluded. Linear regression analyses examined relationships between systolic blood pressure (SBP) and diastolic blood pressure (DBP) at ages 36, 43, 53, 60‐64 and 69 and microstructural metrics at age 69‐71 adjusting for sex, age, socioeconomic class, educational attainment, childhood cognition and antihypertensive medication. Result 379 participants were included (mean age at imaging 70.7 years, 50% female). Higher SBP at ages 53 and 69 was associated with lower FA and NDI; and higher MD, and SBP at 69 was associated with higher ODI. Similarly, higher DBP at ages 53, 60‐64 and 69 were associated with lower FA and NDI; and higher MD. There was no evidence of associations between BP at age 36 or 43 and NAWM diffusion metrics. Conclusion Higher systolic and diastolic blood pressure from age 53 onwards are shown to be associated with differences in diffusion‐based measures of white matter microstructural integrity later in life, suggesting that systolic or diastolic hypertension in over 50’s may contribute to cognitive impairment risk via alterations in NAWM microstructure differences in later life.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S4
    DOI: 10.1002/alz.045707
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 8
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    APOE‐ε4 carriers have superior recall on the ‘What was where?’ visual short‐term memory binding test at age 70, despite a detrimental effect of β‐amyloid : Neuropsychology/Early detection of cognitive decline with neuropsychological tests
    Wiley ; 2020
    In:  Alzheimer's & Dementia Vol. 16, No. S6 ( 2020-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S6 ( 2020-12)
    Abstract: While APOE ‐ε4 carriers are at higher risk of Alzheimer’s disease (AD), there is evidence that APOE ‐ε4 may have some beneficial effects across the life‐span, including on cognition. It is unclear how such effects may relate to subtle memory decline during the preclinical phase of AD. Two previous studies reported that APOE ‐ε4 carriers recalled object locations more accurately than non‐carriers on the “What was where?” visual short‐term memory binding test (10.1016/j.cortex.2016.12.016; 10.1016/j.neurobiolaging.2018.09.017), but these studies did not account for preclinical AD pathology. Method The “What was where?” task (Figure 1) was administered to participants in Insight 46 – a sub‐study of the British 1946 birth cohort – who were all born during the same week (aged 69‐71 at assessment (Table 1)). Outcomes included object identification and a sensitive analogue measure of localisation error (the distance between the location reported by the participant and the true location). Two‐dimensional mixture models (10.31234/osf.io/q57fm) were used to isolate three sources of localisation error: imprecision, guessing, and misbinding (swapping an object’s location with that of a different object). β‐Amyloid status (positive / negative) was determined from 18 F‐Florbetapir‐PET. Multivariable regression models were used to investigate differential effects of APOE genotype (ε4‐carrier / non‐carrier) and β‐amyloid status on performance in 398 cognitively‐normal participants, adjusting for confounders including a prospectively‐collected measure of childhood cognitive ability. Result APOE ‐ε4 and β‐amyloid had opposing effects on object identification, with APOE ‐ε4 predicting better recall and β‐amyloid‐positivity predicting poorer recall. APOE ‐ε4 carriers also recalled object locations more precisely, but a subtle detrimental effect of β‐amyloid on localisation was seen only among non‐carriers (Table 2 , Figure 2). Childhood cognitive ability also predicted performance over 60 years later (Table 2). Conclusion In this large population‐based sample of cognitively‐normal ∼70‐year‐olds, a positive association between APOE ‐ε4 and short‐term visual memory was observed. For the localization measure, this appeared to be protective against a subtle deficit associated with β‐amyloid pathology. This is consistent with the antagonistic pleiotropy hypothesis – whereby a gene controls both beneficial and detrimental traits – and provides novel evidence that these effects persist into older age, even among individuals who may be in the preclinical stages of AD.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v16.S6
    DOI: 10.1002/alz.041090
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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