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Risacher, S. L.

Publications and source records attributed to Risacher, S. L..

12 recordsLinked to original sources

Predicting Autopsy-Confirmed Neuropathology across Clinical, Neuroimaging, and CSF Biomarkers using Machine Learning

Accurate in vivo prediction of neuropathology is critical for advancing diagnosis and treatment of Alzheimers disease and related dementias (ADRDs). As many individuals with ADRDs have mixed pathologies ({beta}-amyloid, pathologic tau, cerebrovascular disease, vascular brain injury, pathologic TDP-43, hippocampal sclerosis, Lewy bodies), there is interest in determining how accurately we can infer these pathologic changes from clinical data, biofluid assays (e.g., CSF), and neuroimaging. Here we evaluated automated machine learning models trained on data curated by the AD Sequencing Project Phenotype Harmonization Consortium (N=7,894 individuals), to predict 26 autopsy-confirmed neuropathological outcomes. Predictors included in vivo clinical and cognitive composite scores, brain measures from 3D structural MRI and diffusion tensor imaging, image-derived measures of white matter hyperintensities (WMH), and CSF biomarkers. Predictive models were trained using ensemble learning with stratified cross-validation. We assessed performance using Spearmans rank correlation and Matthews correlation coefficient, to accommodate co-occurring pathologic changes. The added value of neuroimaging and CSF versus clinical features alone was quantified. Braak stage was among the most consistently predicted outcomes. CSF biomarkers best predicted {beta}-amyloid and tau pathology, but diffusion MRI metrics best captured vascular brain injury and white matter injury, and outperformed clinical and cognitive measures and anatomical MRI in predicting Lewy body disease. Anatomical measures from structural MRI outperformed standard clinical assessments in assessing neurodegeneration and hippocampal sclerosis, and WMH complemented cognitive measures in predicting TDP-43 pathology. These results establish a baseline for comparing modalities for inferring neuropathology.

neuroscience↗

Individualized Mapping of Functional Brain Networks in Older Adulthood

The functional network architecture of the aging brain undergoes significant systematic and idiosyncratic changes. Emergent individualized network mapping approaches may yield better or more sensitive explanatory insight about age-related neural and behavioral variability, although most applications have focused on young adults. In the current study, we tested the validity and impact of mapping individual-specific topography in two fMRI datasets comprising 112 young (18-35 years) and 176 older adults (60-92 years). Older adults had more idiosyncratic network topography than young adults. Individualized maps from resting-state fMRI improved network homogeneity and fidelity to task fMRI activations, while also exhibiting intra-individual reliability and inter-individual discriminability over a 2-year interval. Last, traditional group-averaged (vs. individualized) network mapping had a moderate-to-large impact on individual-level estimates of network segregation, a widely-studied measure of functional brain aging. Therefore, individualized network mapping captures important heterogeneity in older adulthood and may yield more precise characterization of neurocognitive aging.

neuroscience↗

Sex, racial, and APOE-ϵ4 allele differences in longitudinal white matter microstructure in multiple cohorts of aging and Alzheimer's disease

Structured AbstractO_ST_ABSINTRODUCTIONC_ST_ABSThe effects of sex, race, and Apolipoprotein E (APOE) - Alzheimers disease (AD) risk factors - on white matter integrity are not well characterized. METHODSDiffusion MRI data from nine well-established longitudinal cohorts of aging were free-water (FW)-corrected and harmonized. This dataset included 4,702 participants (age=73.06 {+/-} 9.75) with 9,671 imaging sessions over time. FW and FW-corrected fractional anisotropy (FAFWcorr) were used to assess differences in white matter microstructure by sex, race, and APOE-{varepsilon}4 carrier status. RESULTSSex differences in FAFWcorr in association and projection tracts, racial differences in FAFWcorr in projection tracts, and APOE-{varepsilon}4 differences in FW limbic and occipital transcallosal tracts were most pronounced. DISCUSSIONThere are prominent differences in white matter microstructure by sex, race, and APOE- {varepsilon}4 carrier status. This work adds to our understanding of disparities in AD. Additional work to understand the etiology of these differences is warranted. HighlightsO_LISex, race, and APOE-{varepsilon}4 carrier status relate to white matter microstructural integrity C_LIO_LIFemales generally have lower FAFWcorr compared to males C_LIO_LINon-Hispanic Black adults generally have lower FAFWcorr than non-Hispanic White adults C_LIO_LIAPOE-{varepsilon}4 carriers tended to have higher FW than non-carriers C_LI Research in Context Systematic ReviewThe authors used PubMed and Google Scholar to review literature that used conventional and free-water (FW)-corrected microstructural metrics to evaluate sex, race, and APOE-{varepsilon}4 differences in white matter microstructure. While studies have previously explored differences by sex and APOE-{varepsilon}4 status, less is known about racial differences and no large-scale FW-corrected analysis has been performed. InterpretationSex and race were more associated with FAFWcorr while APOE-{varepsilon}4 status was associated with FW metrics. Association, projection, limbic, and occipital transcallosal tracts showed the greatest differences. Future DirectionFuture studies to determine the biological and social pathways that lead to sex, racial, and APOE-{varepsilon}4 differences are warranted. Consent StatementAll participants provided informed consent in their respective cohort studies.

neuroscience↗

Leveraging longitudinal diffusion MRI data to quantify differences in white matter microstructural decline in normal and abnormal aging

AbstractO_ST_ABSINTRODUCTIONC_ST_ABSIt is unclear how rates of white matter microstructural decline differ between normal aging and abnormal aging. METHODSDiffusion MRI data from several well-established longitudinal cohorts of aging [Alzheimers Neuroimaging Initiative (ADNI), Baltimore Longitudinal Study of Aging (BLSA), Vanderbilt Memory & Aging Project (VMAP)] was free-water corrected and harmonized. This dataset included 1,723 participants (age at baseline: 72.8{+/-}8.87 years, 49.5% male) and 4,605 imaging sessions (follow-up time: 2.97{+/-}2.09 years, follow-up range: 1-13 years, mean number of visits: 4.42{+/-}1.98). Differences in white matter microstructural decline in normal and abnormal agers was assessed. RESULTSWhile we found global decline in white matter in normal/abnormal aging, we found that several white matter tracts (e.g., cingulum bundle) were vulnerable to abnormal aging. CONCLUSIONSThere is a prevalent role of white matter microstructural decline in aging, and future large-scale studies in this area may further refine our understanding of the underlying neurodegenerative processes. HIGHLIGHTSO_LILongitudinal data was free-water corrected and harmonized C_LIO_LIGlobal effects of white matter decline were seen in normal and abnormal aging C_LIO_LIThe free-water metric was most vulnerable to abnormal aging C_LIO_LICingulum free-water was the most vulnerable to abnormal aging C_LI

neuroscience↗

Serum Metabolites Associate with Brain Amyloid Beta Deposition, Cognitive Dysfunction, and Alzheimers Disease Progression

RATIONALEMetabolomics in the Alzheimers Disease Neuroimaging Initiative (ADNI) cohort provides a powerful tool for mapping biochemical changes in AD, and a unique opportunity to learn about the association between circulating blood metabolites and brain amyloid-{beta} deposition in AD. OBJECTIVESWe examined 140 serum metabolites and their associations with brain amyloid-{beta} deposition, cognition, and conversion from mild cognitive impairment (MCI) to AD. FINDINGSSerum-based targeted metabolite levels were measured in 1,531 ADNI participants. We performed association analysis of metabolites with brain amyloid-{beta} deposition measured from [18F] Florbetapir PET scans. We identified nine metabolites as significantly associated with amyloid-{beta} deposition after FDR-based multiple comparison correction. Higher levels of one acylcarnitine (C3; propionylcarnitine) and one biogenic amine (kynurenine) were associated with decreased amyloid-{beta} accumulation. However, higher levels of seven phosphatidylcholines (PC) were associated with increased amyloid deposition. In addition, PC ae C44:4 was significantly associated with cognition and conversion from MCI to AD dementia. CONCLUSIONPerturbations in PC and acylcarnitine metabolism may play a role in features intrinsic to AD including amyloid-{beta} deposition and cognitive performance.

neuroscience↗

Differential brain atrophy and neurogenetic profiles in cognitively-defined Alzheimer's disease subgroups

Elucidating mechanisms underlying the clinical heterogeneity observed among individuals with Alzheimers disease (AD) is key to facilitate personalized treatments. We categorized 679 individuals with AD into subgroups based on a relative impairment in one cognitive domain (i.e. AD-Memory, AD-Executive-Functioning, AD-Language and AD-Visuospatial-Functioning). We compared atrophy patterns derived from MRI and identified patterns that closely matched the respective cognitive profiles, i.e. medial temporal lobe atrophy in AD-Memory, fronto-parietal in AD-Executive-Functioning, asymmetric left-temporal in AD-Language, and posterior in AD-Visuospatial-Functioning. We then determined spatial correlations between subgroup-specific atrophy and a transcriptomic atlas of gene expression, which revealed both shared (e.g. mitochondrial respiration and synaptic function/plasticity) and subgroup-specific (e.g. cell-cycle for AD-Memory, protein metabolism in AD-Language, and modification of gene expression in AD-Visuospatial-Functioning) biological pathways associated with each subgroups atrophy patterns. We conclude that cognitive heterogeneity in AD is related to neuroanatomical differences, and specific biological pathways may be involved in their emergence.

neuroscience↗

Deep learning detection of informative features in tau PET for Alzheimer' s disease classification

BackgroundAlzheimers disease (AD) is the most common type of dementia, typically characterized by memory loss followed by progressive cognitive decline and functional impairment. Many clinical trials of potential therapies for AD have failed, and there is currently no approved disease-modifying treatment. Biomarkers for early detection and mechanistic understanding of disease course are critical for drug development and clinical trials. Amyloid has been the focus of most biomarker research. Here, we developed a deep learning-based framework to identify informative features for AD classification using tau positron emission tomography (PET) scans. MethodsWe analysed [18F]flortaucipir PET image data from the Alzheimers Disease Neuroimaging Initiative (ADNI) cohort. We first developed an image classifier to distinguish AD from cognitively normal (CN) older adults by training a 3D convolutional neural network (CNN)-based deep learning model on tau PET images (N=132; 66 CN and 66 AD), then applied the classifier to images from individuals with mild cognitive impairment (MCI; N=168). In addition, we applied a layer-wise relevance propagation (LRP)-based model to identify informative features and to visualize classification results. We compared these results with those from whole brain voxel-wise between-group analysis using conventional Statistical Parametric Mapping (SPM12). ResultsThe 3D CNN-based classification model of AD from CN yielded an average accuracy of 90.8% based on five-fold cross-validation. The LRP model identified the brain regions in tau PET images that contributed most to the AD classification from CN. The top identified regions included the hippocampus, parahippocampus, thalamus, and fusiform. The LRP results were consistent with those from the voxel-wise analysis in SPM12, showing significant focal AD associated regional tau deposition in the bilateral temporal lobes including the entorhinal cortex. The AD probability scores calculated by the classifier were correlated with brain tau deposition in the medial temporal lobe in MCI participants (r=0.43 for early MCI and r=0.49 for late MCI). ConclusionA deep learning framework combining 3D CNN and LRP algorithms can be used with tau PET images to identify informative features for AD classification and may have application for early detection during prodromal stages of AD.

neuroscience↗

Elevated plasma cortisol associated with larger ventricles and smaller hippocampal volumes, a study in 2 independent elderly cohorts

Cortisol is considered the most fundamental stress hormone and is elevated in stress and multiple neuropsychiatric conditions. Prior studies have shown associations of plasma cortisol levels with total cerebral and hippocampal volumes and less consistently with the amygdala. Here, we extend our hypothesis to test associations of plasma cortisol with 1) ventricular 2) hippocampal and 3) amygdalar volumes, in two independent elderly cohorts across a broad cognitive spectrum ranging from normal cognition to Alzheimers disease. We demonstrate elevated cortisol to be associated with larger lateral ventricular volumes and smaller hippocampal volumes, predominantly in the right cerebral hemisphere, regardless of age, sex or cognitive status. We noted a non-significant trend of smaller amygdalar volumes with elevated cortisol. Our findings support smaller brain parenchyma volumes seen with elevated cortisol and may encourage effective strategies reducing cortisol and stress. They may also serve as imaging biomarkers for assessing therapeutic benefits of stress and cortisol lowering interventions aiming to halt or reverse the brain volume alterations and theoretically improve cognition and quality of life. HighlightsO_LIElevated cortisol associated with larger ventricular volumes and smaller hippocampal volumes C_LIO_LIAssociations are predominantly noted in the right cerebral hemisphere. C_LIO_LISimilar non-significant trends noted in amygdalar volumes C_LIO_LICortisol and stress reducing strategies may halt brain changes and improve quality of life C_LIO_LIImaging biomarkers may help assess efficacy of cortisol-lowering therapeutic interventions C_LI

neuroscience↗

Functional biological paths altered in Alzheimer's disease: from genes to bile acids

Large-scale genome wide association studies (GWASs) have been performed in search for risk genes for Alzheimers disease (AD). Despite the significant progress, replicability of genetic findings and their translation into targetable mechanisms related to the disease pathogenesis remains a challenge. Given that bile acids have been suggested in recent metabolic studies as potential age-related metabolic factors associated with AD, we integrated genomic and metabolomic data together with heterogeneous biological networks and investigated the potential cascade of effect of genetic variations to proteins, bile acids and ultimately AD brain phenotypes. Particularly, we leveraged functional protein interaction networks and metabolic networks and focused on the genes directly interacting with AD-altered bile acids and their functional regulators. We examined the association of all the SNPs located in those candidate genes with AD brain imaging phenotypes, and identified multiple AD risk SNPs whose downstream genes and bile acids were also found to be altered in AD. These AD related markers span from genetics to metabolomics, forming functional biological paths connecting across multiple-omics layers, and give valuable insights into the underlying mechanism of AD.

bioinformatics↗

Neuropathological correlates and genetic architecture of microglial activation in elderly human brain

Microglia, the resident immune cells of the brain, have important roles in brain health. However, little is known about the regulation and consequences of microglial activation in the aging human brain. We assessed the effect of microglial activation in the aging human brain by calculating the proportion of activated microglia (PAM), based on morphologically defined stages of activation in four regions sampled postmortem from up to 225 elderly individuals. We found that cortical and not subcortical PAM measures were strongly associated with {beta}-amyloid, tau-related neuropathology, and rates of cognitive decline. Effect sizes for PAM measures are substantial, comparable to that of APOE {varepsilon}4, the strongest genetic risk factor for Alzheimers disease. Mediation modeling suggests that PAM accelerates accumulation of tau pathology leading to cognitive decline, supporting an upstream role for microglial activation in Alzheimers disease. Genome-wide analyses identified a common variant (rs2997325) influencing cortical PAM that also affected in vivo microglial activation measured by positron emission tomography using [11C]-PBR28 in an independent cohort. Finally, we identify overlaps of PAMs genetic architecture with those of Alzheimers disease, educational attainment, and several other traits.

genomics↗

Altered Bile Acid Profile in Mild Cognitive Impairment and Alzheimer’s Disease: Relationship to Neuroimaging and CSF Biomarkers

IntroductionBile acids (BAs) are the end products of cholesterol metabolism produced by human and gut microbiome co-metabolism. Recent evidence suggests gut microbiota influence pathological features of Alzheimers disease (AD) including neuroinflammation and amyloid-{beta} deposition.\n\nMethodSerum levels of 20 primary and secondary BA metabolites from the AD Neuroimaging Initiative (n=1562) were measured using targeted metabolomic profiling. We assessed the association of BAs with the \"A/T/N\" (Amyloid, Tau and Neurodegeneration) biomarkers for AD: CSF biomarkers, atrophy (MRI), and brain glucose metabolism ([18F]FDG-PET).\n\nResultsOf 23 BA and relevant calculated ratios, three BA signatures were associated with CSF A{beta}1-42 (\"A\") and three with CSF p-tau181 (\"T\") (corrected p<0.05). Furthermore, three, twelve, and fourteen BA signatures were associated with CSF t-tau, glucose metabolism, and atrophy (\"N\"), respectively (corrected p<0.05).\n\nConclusionThis is the first study to show serum-based BA metabolites are associated with \"A/T/N\" AD biomarkers, providing further support for a role of BA pathways in AD pathophysiology. Prospective clinical observations and validation in model systems are needed to assess causality and specific mechanisms underlying this association.

neuroscience↗

Altered Bile Acid Profile Associates with Cognitive Impairment in Alzheimer’s Disease – An Emerging Role for Gut Microbiome

IntroductionIncreasing evidence suggests a role for the gut microbiome in central nervous system disorders and specific role for the gut-brain axis in neurodegeneration. Bile acids (BA), products of cholesterol metabolism and clearance, are produced in the liver and are further metabolized by gut bacteria. They have major regulatory and signaling functions and seem dysregulated in Alzheimer disease (AD).\n\nMethodsSerum levels of 15 primary and secondary BAs and their conjugated forms were measured in 1,464 subjects including 370 cognitively normal older adults (CN), 284 with early mild cognitive impairment (MCI), 505 with late MCI, and 305 AD cases enrolled in the AD Neuroimaging Initiative. We assessed associations of BA profiles including selected ratios with diagnosis, cognition, and AD-related genetic variants, adjusting for cofounders and multiple testing.\n\nResultsIn AD compared to CN, we observed significantly lower serum concentrations of a primary BA (cholic acid CA) and increased levels of the bacterially produced, secondary BA, deoxycholic acid (DCA), and its glycine and taurine conjugated forms. An increased ratio of DCA:CA, which reflects 7-dehydroxylation of CA by gut bacteria, strongly associated with cognitive decline, a finding replicated in serum and brain samples in the Rush Religious Orders and Memory and Aging Project. Several genetic variants in immune response related genes implicated in AD showed associations with BA profiles.\n\nConclusionWe report for the first time an association between altered BA profile, genetic variants implicated in AD and cognitive changes in disease using a large multicenter study. These findings warrant further investigation of gut dysbiosis and possible role of gut liver brain axis in the pathogenesis of AD.

neuroscience↗