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Article ; Online: Association of β-Amyloid and Vascular Risk on Longitudinal Patterns of Brain Atrophy.

Rabin, Jennifer S / Pruzin, Jeremy / Scott, Matthew / Yang, Hyun-Sik / Hampton, Olivia / Hsieh, Stephanie / Schultz, Aaron P / Buckley, Rachel F / Hedden, Trey / Rentz, Dorene / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P

Neurology

2022 Volume 99, Issue 3, Page(s) e270–e280

Abstract: Background and objectives: Vascular risk factors and elevated β-amyloid (Aβ) are commonly observed together among older adults. Here, we examined the interactive vs independent effects of systemic vascular risk and Aβ burden on longitudinal gray matter ... ...

Abstract	Background and objectives: Vascular risk factors and elevated β-amyloid (Aβ) are commonly observed together among older adults. Here, we examined the interactive vs independent effects of systemic vascular risk and Aβ burden on longitudinal gray matter atrophy and how their co-occurrence may be related to cognitive decline in a cohort of clinically normal adults. A secondary goal was to examine whether vascular risk influences gray matter atrophy independently from markers of white matter injury. Methods: Participants were 196 adults (age 73.8 ± 6.1 years) from the Harvard Aging Brain Study. Baseline Aβ burden was quantified with Pittsburgh compound B PET. Baseline vascular risk was measured with the Framingham Heart Study cardiovascular disease risk score. Brain atrophy was quantified longitudinally with structural MRI over a median of 4.50 (±1.26) years. Cognition was assessed yearly with the Preclinical Alzheimer Cognitive Composite over a median of 6.25 (±1.40) years. Linear mixed-effects models examined vascular risk and Aβ burden as interactive vs independent predictors of gray matter atrophy, with adjustment for age, sex, years of education, Results: Higher vascular risk and elevated Aβ burden interacted to predict more severe atrophy in frontal and temporal lobes, thalamus, and striatum. Higher Aβ burden, but not vascular risk, was associated with more severe atrophy in parietal and occipital lobes, as well as the hippocampus. Adjusting for diffusion- and FLAIR-based markers of white matter injury had little impact on the above associations. Gray matter atrophy mediated the association between vascular risk and cognitive decline at higher levels of Aβ burden. Discussion: We observed an interaction between elevated vascular risk and higher Aβ burden with longitudinal brain atrophy, which in turn influenced cognitive decline. These results support vascular risk factor management as a potential intervention to slow neurodegeneration and cognitive decline in preclinical Alzheimer disease.
MeSH term(s)	Humans ; Aged ; Amyloid beta-Peptides/metabolism ; Brain/pathology ; Alzheimer Disease/pathology ; Gray Matter/pathology ; Cognitive Dysfunction/diagnostic imaging ; Cognitive Dysfunction/pathology ; Longitudinal Studies ; Magnetic Resonance Imaging ; Atrophy/pathology ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2022-07-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000200551
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Article ; Online: Harmonizing the preclinical Alzheimer cognitive composite for multicohort studies.

Hampton, Olivia L / Mukherjee, Shubhabrata / Properzi, Michael J / Schultz, Aaron P / Crane, Paul K / Gibbons, Laura E / Hohman, Timothy J / Maruff, Paul / Lim, Yen Ying / Amariglio, Rebecca E / Papp, Kathryn V / Johnson, Keith A / Rentz, Dorene M / Sperling, Reisa A / Buckley, Rachel F

Neuropsychology

2022 Volume 37, Issue 4, Page(s) 436–449

Abstract: Objectives: Studies are increasingly examining research questions across multiple cohorts using data from the preclinical Alzheimer cognitive composite (PACC). Our objective was to use modern psychometric approaches to develop a harmonized PACC.: ... ...

Abstract	Objectives: Studies are increasingly examining research questions across multiple cohorts using data from the preclinical Alzheimer cognitive composite (PACC). Our objective was to use modern psychometric approaches to develop a harmonized PACC. Method: We used longitudinal data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), Harvard Aging Brain Study (HABS), and Australian Imaging, Biomarker and Lifestyle Study of Ageing (AIBL) cohorts ( Results: Baseline (BL) scores for the zPACC were centered on zero, by definition. The harmonized lPACC did not define a common mean of zero and demonstrated differences in baseline ability levels across the cohorts. Baseline lPACC slightly outperformed zPACC in the prediction of progression to dementia. Longitudinal change in the lPACC was more constrained and less variable relative to the zPACC. In combined-cohort analyses, longitudinal lPACC slightly outperformed longitudinal zPACC in its association with baseline β-amyloid status. Conclusions: This study proposes procedures for harmonizing the PACC that make fewer strong assumptions than the zPACC, facilitating robust multicohort analyses. This implementation of item response theory lends itself to adapting across future cohorts with similar composites. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
MeSH term(s)	Humans ; Alzheimer Disease/psychology ; Cognitive Dysfunction/psychology ; Disease Progression ; Australia ; Amyloid beta-Peptides ; Biomarkers ; Cognition ; Longitudinal Studies
Chemical Substances	Amyloid beta-Peptides ; Biomarkers
Language	English
Publishing date	2022-07-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1042412-x
ISSN	1931-1559 ; 0894-4105
ISSN (online)	1931-1559
ISSN	0894-4105
DOI	10.1037/neu0000833
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Article ; Online: Inferior temporal tau is associated with accelerated prospective cortical thinning in clinically normal older adults.

Scott, Matthew R / Hampton, Olivia L / Buckley, Rachel F / Chhatwal, Jasmeer P / Hanseeuw, Bernard J / Jacobs, Heidi Il / Properzi, Michael J / Sanchez, Justin S / Johnson, Keith A / Sperling, Reisa A / Schultz, Aaron P

NeuroImage

2020 Volume 220, Page(s) 116991

Abstract: Neurofibrillary tau tangles are a hallmark pathology of Alzheimer's disease (AD) and are more closely associated with AD-related cortical atrophy and symptom severity than amyloid-beta (Aβ). However, studies regarding the effect of tau on longitudinal ... ...

Abstract	Neurofibrillary tau tangles are a hallmark pathology of Alzheimer's disease (AD) and are more closely associated with AD-related cortical atrophy and symptom severity than amyloid-beta (Aβ). However, studies regarding the effect of tau on longitudinal cortical thinning, particularly in healthy aging and preclinical AD, have been limited in number due to the relatively recent introduction of in vivo PET tracers for imaging tau pathology. Here, we investigate [18F]-flortaucipir (FTP, a marker of paired helical filament tau) PET as a predictor of atrophy in healthy aging and preclinical AD. We examine longitudinal structural MRI brain imaging data, retrospectively and prospectively relative to FTP imaging, using piecewise linear mixed-effect models with time centered at each participant's FTP-PET session. Participants include 111 individuals from the Harvard Aging Brain Study who underwent at least three MRI sessions over an average of 4.46 years and one FTP-PET at the approximate midpoint of the observation period. Our primary analyses focus on inferior temporal (IT) FTP standardized uptake value ratios and longitudinal FreeSurfer defined cortical regions of interest. Relationships were also explored using other regional FTP measures (entorhinal, composite, and local), within high and low Pittsburgh compound-B (PiB) PET groups, and with longitudinal subcortical volume. Strong associations between IT FTP and cortical thinning were found, most notably in temporal, midline, and prefrontal regions, with stronger effects generally observed in the prospective as compared to retrospective time frame. Significant differences between prospective and retrospective rates of thinning were found in the inferior and middle temporal gyri, cingulate areas, as well as pars orbitalis such that higher IT FTP was associated with greater prospective rates of thinning. Within the high PiB group, significant differences between prospective and retrospective rates of thinning were similarly observed. However, no consistent pattern of tau-related change in cortical thickness within the low PiB group was discerned. These results provide support for the hypothesis that tau pathology is a driver of future atrophy as well as provide additional evidence for tau-PET as an effective AD biomarker for interventional clinical trials.
MeSH term(s)	Aged ; Aging/metabolism ; Aging/pathology ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Brain/diagnostic imaging ; Brain/metabolism ; Brain/pathology ; Cerebral Cortex/diagnostic imaging ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cerebral Cortical Thinning/diagnostic imaging ; Cerebral Cortical Thinning/metabolism ; Cerebral Cortical Thinning/pathology ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Models, Neurological ; Neurofibrillary Tangles/metabolism ; Neurofibrillary Tangles/pathology ; Positron-Emission Tomography ; Retrospective Studies ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; tau Proteins
Language	English
Publishing date	2020-06-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1147767-2
ISSN	1095-9572 ; 1053-8119
ISSN (online)	1095-9572
ISSN	1053-8119
DOI	10.1016/j.neuroimage.2020.116991
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Article ; Online: Resting-state functional connectivity and amyloid burden influence longitudinal cortical thinning in the default mode network in preclinical Alzheimer's disease.

Hampton, Olivia L / Buckley, Rachel F / Manning, Lyssa K / Scott, Matthew R / Properzi, Michael J / Peña-Gómez, Cleofé / Jacobs, Heidi I L / Chhatwal, Jasmeer P / Johnson, Keith A / Sperling, Reisa A / Schultz, Aaron P

NeuroImage. Clinical

2020 Volume 28, Page(s) 102407

Abstract: Proteinopathies are key elements in the pathogenesis of age-related neurodegenerative diseases, particularly Alzheimer's disease (AD), with the nature and location of the proteinopathy characterizing much of the disease phenotype. Susceptibility of brain ...

Abstract	Proteinopathies are key elements in the pathogenesis of age-related neurodegenerative diseases, particularly Alzheimer's disease (AD), with the nature and location of the proteinopathy characterizing much of the disease phenotype. Susceptibility of brain regions to pathology may partly be determined by intrinsic network structure and connectivity. It remains unknown, however, how these networks inform the disease cascade in the context of AD biomarkers, such as beta-amyloid (Aβ), in clinically-normal older adults.The default-mode network (DMN), a prominent intrinsic network, is heavily implicated in AD due to its spatial overlap with AD atrophy patterns and tau deposition. We investigated the influence of baseline Aβ positron emission tomography (PET) signal and intrinsic DMN connectivity on DMN-specific cortical thinning in 120 clinically-normal older adults from the Harvard Aging Brain Study (73 ± 6 years, 58% Female, CDR = 0). Participants underwent
MeSH term(s)	Aged ; Alzheimer Disease/diagnostic imaging ; Amyloid beta-Peptides/metabolism ; Brain/diagnostic imaging ; Brain/metabolism ; Cerebral Cortical Thinning ; Default Mode Network ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Positron-Emission Tomography ; Tomography, X-Ray Computed
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2020-09-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701571-3
ISSN	2213-1582 ; 2213-1582
ISSN (online)	2213-1582
ISSN	2213-1582
DOI	10.1016/j.nicl.2020.102407
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Article ; Online: Longitudinal degradation of the default/salience network axis in symptomatic individuals with elevated amyloid burden.

Schultz, Aaron P / Buckley, Rachel F / Hampton, Olivia L / Scott, Matthew R / Properzi, Michael J / Peña-Gómez, Cleofé / Pruzin, Jeremy J / Yang, Hyun-Sik / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P

NeuroImage. Clinical

2019 Volume 26, Page(s) 102052

Abstract: Resting-state functional connectivity MRI (rs-fcMRI) is a non-invasive imaging technique that has come into increasing use to understand disrupted neural network function in neuropsychiatric disease. However, despite extensive study over the past 15 ... ...

Abstract	Resting-state functional connectivity MRI (rs-fcMRI) is a non-invasive imaging technique that has come into increasing use to understand disrupted neural network function in neuropsychiatric disease. However, despite extensive study over the past 15 years, the development of rs-fcMRI as a biomarker has been impeded by a lack of reliable longitudinal rs-fcMRI measures. Here we focus on longitudinal change along the Alzheimer's disease (AD) trajectory and demonstrate the utility of Template Based Rotation (TBR) in detecting differential longitudinal rs-fcMRI change between higher and lower amyloid burden individuals with mildly impaired cognition. Specifically, we examine a small (N = 24), but densely sampled (~5 observations over ~3 years), cohort of symptomatic individuals with serial rs-fcMRI imaging and PiB-PET imaging for β-amyloid pathology. We observed longitudinal decline of the Default Mode and Salience network axis (DMN/SAL) among impaired individuals with high amyloid burden. No other networks showed differential change in high vs. low amyloid individuals over time. The standardized effect size of AD related DMN/SAL change is comparable to the standardized effect size of amyloid-related change on the mini-mental state exam (MMSE) and hippocampal volume (HV). Last, we show that the AD-related change in DMN/SAL connectivity is almost completely independent of change on MMSE or HV, suggesting that rs-fcMRI is sensitive to an aspect of AD progression that is not captured by these other measures. Together these analyses demonstrate that longitudinal rs-fcMRI using TBR can capture disease-relevant network disruption in a clinical population.
MeSH term(s)	Aged ; Aged, 80 and over ; Amyloid beta-Peptides/metabolism ; Brain/diagnostic imaging ; Brain/metabolism ; Brain/physiopathology ; Cognitive Dysfunction/diagnostic imaging ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/physiopathology ; Connectome ; Female ; Humans ; Longitudinal Studies ; Magnetic Resonance Imaging ; Male ; Mental Status and Dementia Tests ; Nerve Net/diagnostic imaging ; Nerve Net/physiopathology ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2019-10-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701571-3
ISSN	2213-1582 ; 2213-1582
ISSN (online)	2213-1582
ISSN	2213-1582
DOI	10.1016/j.nicl.2019.102052
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Article ; Online: In vivo and neuropathology data support locus coeruleus integrity as indicator of Alzheimer's disease pathology and cognitive decline.

Jacobs, Heidi I L / Becker, John A / Kwong, Kenneth / Engels-Domínguez, Nina / Prokopiou, Prokopis C / Papp, Kathryn V / Properzi, Michael / Hampton, Olivia L / d'Oleire Uquillas, Federico / Sanchez, Justin S / Rentz, Dorene M / El Fakhri, Georges / Normandin, Marc D / Price, Julie C / Bennett, David A / Sperling, Reisa A / Johnson, Keith A

Science translational medicine

2021 Volume 13, Issue 612, Page(s) eabj2511

Abstract: Several autopsy studies recognize the locus coeruleus (LC) as the initial site of hyperphosphorylated TAU aggregation, and as the number of LC neurons harboring TAU increases, TAU pathology emerges throughout the cortex. By conjointly using dedicated MRI ...

Abstract	Several autopsy studies recognize the locus coeruleus (LC) as the initial site of hyperphosphorylated TAU aggregation, and as the number of LC neurons harboring TAU increases, TAU pathology emerges throughout the cortex. By conjointly using dedicated MRI measures of LC integrity and TAU and amyloid PET imaging, we aimed to address the question whether in vivo LC measures relate to initial cortical patterns of Alzheimer’s disease (AD) fibrillar proteinopathies or cognitive dysfunction in 174 cognitively unimpaired and impaired older individuals with longitudinal cognitive measures. To guide our interpretations, we verified these associations in autopsy data from 1524 Religious Orders Study and Rush Memory and Aging Project and 2145 National Alzheimer’s Coordinating Center cases providing three different LC measures (pigmentation, tangle density, and neuronal density), Braak staging, β-amyloid, and longitudinal cognitive measures. Lower LC integrity was associated with elevated TAU deposition in the entorhinal cortex among unimpaired individuals consistent with postmortem correlations between LC tangle density and successive Braak staging. LC pigmentation ratings correlated with LC neuronal density but not with LC tangle density and were particularly worse at advanced Braak stages. In the context of elevated β-amyloid, lower LC integrity and greater cortical tangle density were associated with greater TAU burden beyond the medial temporal lobe and retrospective memory decline. These findings support neuropathologic data in which early LC TAU accumulation relates to disease progression and identify LC integrity as a promising indicator of initial AD-related processes and subtle changes in cognitive trajectories of preclinical AD.
MeSH term(s)	Alzheimer Disease ; Cognitive Dysfunction ; Humans ; Locus Coeruleus ; Neuropathology
Language	English
Publishing date	2021-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abj2511
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Article: Evaluation of Electronic Effects in the Solvolyses of

D'Souza, Malcolm J / Hampton, Olivia N / Sansbury, Brett M / Kevill, Dennis N

Journal of chemistry

2013 Volume 2013

Abstract: The solvolyses ... ...

Abstract	The solvolyses of
Language	English
Publishing date	2013-11-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2703077-5
ISSN	2090-9071 ; 2090-9063
ISSN (online)	2090-9071
ISSN	2090-9063
DOI	10.1155/2013/248534
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Article: Cortical thickness across the lifespan in a Colombian cohort with autosomal-dominant Alzheimer's disease: A cross-sectional study.

Fox-Fuller, Joshua T / Torrico-Teave, Heirangi / d'Oleire Uquillas, Federico / Chen, Kewei / Su, Yi / Chen, Yinghua / Brickhouse, Michael / Sanchez, Justin S / Aguero, Cinthya / Jacobs, Heidi I L / Hampton, Olivia / Guzmán-Vélez, Edmarie / Vila-Castelar, Clara / Aguirre-Acevedo, Daniel C / Baena, Ana / Artola, Arabiye / Martinez, Jairo / Pluim, Celina F / Alvarez, Sergio /

Ochoa-Escudero, Martin / Reiman, Eric M / Sperling, Reisa A / Lopera, Francisco / Johnson, Keith A / Dickerson, Bradford C / Quiroz, Yakeel T

Alzheimer's & dementia (Amsterdam, Netherlands)

2021 Volume 13, Issue 1, Page(s) e12233

Abstract: Introduction: Cortical thinning is a marker of neurodegeneration in Alzheimer's disease (AD). We investigated the age-related trajectory of cortical thickness across the lifespan (9-59 years) in a Colombian kindred with autosomal dominant AD (ADAD).: ... ...

Abstract	Introduction: Cortical thinning is a marker of neurodegeneration in Alzheimer's disease (AD). We investigated the age-related trajectory of cortical thickness across the lifespan (9-59 years) in a Colombian kindred with autosomal dominant AD (ADAD). Methods: Two hundred eleven participants (105 presenilin-1 [ Results: Unimpaired carriers exhibited elevated cortical thickness compared to non-carriers, and thickness more negatively correlated with age and cognition in carriers relative to non-carriers. We found increased cortical thickness in child carriers, after which thickness steadied compared to non-carriers prior to a rapid reduction in the decade leading up to the expected age at cognitive impairment in carriers. Discussion: Findings suggest that cortical thickness may fluctuate across the ADAD lifespan, from early-life increased thickness to atrophy proximal to clinical onset.
Language	English
Publishing date	2021-09-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832898-X
ISSN	2352-8729
ISSN	2352-8729
DOI	10.1002/dad2.12233
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Article ; Online: Associations of Physical Activity and β-Amyloid With Longitudinal Cognition and Neurodegeneration in Clinically Normal Older Adults.

JAMA neurology

2019 Volume 76, Issue 10, Page(s) 1203–1210

Abstract: Importance: In the absence of disease-modifying therapies for Alzheimer disease, there is a critical need to identify modifiable risk factors that may delay the progression of Alzheimer disease.: Objective: To examine whether physical activity ... ...

Abstract	Importance: In the absence of disease-modifying therapies for Alzheimer disease, there is a critical need to identify modifiable risk factors that may delay the progression of Alzheimer disease. Objective: To examine whether physical activity moderates the association of β-amyloid (Aβ) burden with longitudinal cognitive decline and neurodegeneration in clinically normal individuals and to examine whether these associations are independent of vascular risk. Design, setting, and participants: This longitudinal observational study included clinically normal participants from the Harvard Aging Brain Study. Participants were required to have baseline Aβ positron emission tomography data, baseline medical data to quantify vascular risk, and longitudinal neuropsychological and structural magnetic resonance imaging data. Data were collected from April 2010 to June 2018. Data were analyzed from August to December 2018. Main outcomes and measures: Baseline physical activity was quantified with a pedometer (mean steps per day). Baseline Aβ burden was measured with carbon 11-labeled Pittsburgh Compound B positron emission tomography. Cognition was measured annually with the Preclinical Alzheimer Cognitive Composite (PACC; median [interquartile range] follow-up, 6.0 [4.3-6.3] years). Neurodegeneration was assessed with longitudinal structural magnetic resonance imaging (2 to 5 scans per participant; median [interquartile range] follow-up, 4.5 [3.0-5.0] years), with a focus on total gray matter volume and regional cortical thickness. Physical activity and Aβ burden were examined as interactive predictors of PACC decline and volume loss in separate linear mixed models, adjusting for age, sex, education, apolipoprotein E ε4 status, and, where appropriate, intracranial volume. Secondary models adjusted for vascular risk and its interaction with Aβ burden. Results: Of the 182 included participants, 103 (56.6%) were female, and the mean (SD) age was 73.4 (6.2) years. In models examining PACC decline and volume loss, there was a significant interaction of physical activity with Aβ burden, such that greater physical activity was associated with slower Aβ-related cognitive decline (β, 0.03; 95% CI, 0.02-0.05; P < .001) and volume loss (β, 482.07; 95% CI, 189.40-774.74; P = .002). Adjusting for vascular risk did not alter these associations. In these models, lower vascular risk was independently associated with slower Aβ-related PACC decline (β, -0.04; 95% CI, -0.06 to -0.02; P < .001) and volume loss (β, -483.41; 95% CI, -855.63 to -111.20; P = .01). Conclusions and relevance: Greater physical activity and lower vascular risk independently attenuated the negative association of Aβ burden with cognitive decline and neurodegeneration in asymptomatic individuals. These findings suggest that engaging in physical activity and lowering vascular risk may have additive protective effects on delaying the progression of Alzheimer disease.
Language	English
Publishing date	2019-07-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2019.1879
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