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Article: Altered resting-state functional connectivity and dynamic network properties in cognitive impairment: an independent component and dominant-coactivation pattern analyses study.

Bergamino, Maurizio / Burke, Anna / Sabbagh, Marwan N / Caselli, Richard J / Baxter, Leslie C / Stokes, Ashley M

2024 Volume 16, Page(s) 1362613

Abstract: Introduction: Cognitive impairment (CI) due to Alzheimer's disease (AD) encompasses a decline in cognitive abilities and can significantly impact an individual's quality of life. Early detection and intervention are crucial in managing CI, both in the ... ...

Abstract	Introduction: Cognitive impairment (CI) due to Alzheimer's disease (AD) encompasses a decline in cognitive abilities and can significantly impact an individual's quality of life. Early detection and intervention are crucial in managing CI, both in the preclinical and prodromal stages of AD prior to dementia. Methods: In this preliminary study, we investigated differences in resting-state functional connectivity and dynamic network properties between 23 individual with CI due to AD based on clinical assessment and 15 healthy controls (HC) using Independent Component Analysis (ICA) and Dominant-Coactivation Pattern (d-CAP) analysis. The cognitive status of the two groups was also compared, and correlations between cognitive scores and d-CAP switching probability were examined. Results: Results showed comparable numbers of d-CAPs in the Default Mode Network (DMN), Executive Control Network (ECN), and Frontoparietal Network (FPN) between HC and CI groups. However, the Visual Network (VN) exhibited fewer d-CAPs in the CI group, suggesting altered dynamic properties of this network for the CI group. Additionally, ICA revealed significant connectivity differences for all networks. Spatial maps and effect size analyses indicated increased coactivation and more synchronized activity within the DMN in HC compared to CI. Furthermore, reduced switching probabilities were observed for the CI group in DMN, VN, and FPN networks, indicating less dynamic and flexible functional interactions. Discussion: The findings highlight altered connectivity patterns within the DMN, VN, ECN, and FPN, suggesting the involvement of multiple functional networks in CI. Understanding these brain processes may contribute to developing targeted diagnostic and therapeutic strategies for CI due to AD.
Language	English
Publishing date	2024-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2024.1362613
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Article ; Online: Unbalanced Sample Size Introduces Spurious Correlations to Genome-Wide Heterozygosity Analyses.

Liu, Li / Caselli, Richard J

Human heredity

2020 Volume 84, Issue 4-5, Page(s) 197–202

Abstract: Excess of heterozygosity (H) is a widely used measure of genetic diversity of a population. As high-throughput sequencing and genotyping data become readily available, it has been applied to investigating the associations of genome-wide genetic diversity ...

Abstract	Excess of heterozygosity (H) is a widely used measure of genetic diversity of a population. As high-throughput sequencing and genotyping data become readily available, it has been applied to investigating the associations of genome-wide genetic diversity with human diseases and traits. However, these studies often report contradictory results. In this paper, we present a meta-analysis of five whole-exome studies to examine the association of H scores with Alzheimer's disease. We show that the mean H score of a group is not associated with the disease status, but ot is associated with the sample size. Across all five studies, the group with more samples has a significantly lower H score than the group with fewer samples. To remove potential confounders in empirical data sets, we perform computer simulations to create artificial genomes controlled for the number of polymorphic loci, the sample size, and the allele frequency. Analyses of these simulated data confirm the negative correlation between the sample size and the H score. Furthermore, we find that genomes with a large number of rare variants also have inflated H scores. These biases altogether can lead to spurious associations between genetic diversity and the phenotype of interest. Based on these findings, we advocate that studies shall balance the sample sizes when using genome-wide H scores to assess genetic diversities of different populations, which helps improve the reproducibility of future research.
Language	English
Publishing date	2020-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2424-7
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000507576
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Article ; Online: Combining Blood-Based Biomarkers and Structural MRI Measurements to Distinguish Persons with and without Significant Amyloid Plaques.

Chen, Yanxi / Su, Yi / Wu, Jianfeng / Chen, Kewei / Atri, Alireza / Caselli, Richard J / Reiman, Eric M / Wang, Yalin

Journal of Alzheimer's disease : JAD

2024 Volume 98, Issue 4, Page(s) 1415–1426

Abstract: Background: Amyloid-β (Aβ) plaques play a pivotal role in Alzheimer's disease. The current positron emission tomography (PET) is expensive and limited in availability. In contrast, blood-based biomarkers (BBBMs) show potential for characterizing Aβ ... ...

Abstract	Background: Amyloid-β (Aβ) plaques play a pivotal role in Alzheimer's disease. The current positron emission tomography (PET) is expensive and limited in availability. In contrast, blood-based biomarkers (BBBMs) show potential for characterizing Aβ plaques more affordably. We have previously proposed an MRI-based hippocampal morphometry measure to be an indicator of Aβ plaques. Objective: To develop and validate an integrated model to predict brain amyloid PET positivity combining MRI feature and plasma Aβ42/40 ratio. Methods: We extracted hippocampal multivariate morphometry statistics from MR images and together with plasma Aβ42/40 trained a random forest classifier to perform a binary classification of participant brain amyloid PET positivity. We evaluated the model performance using two distinct cohorts, one from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the other from the Banner Alzheimer's Institute (BAI), including prediction accuracy, precision, recall rate, F1 score, and AUC score. Results: Results from ADNI (mean age 72.6, Aβ+ rate 49.5%) and BAI (mean age 66.2, Aβ+ rate 36.9%) datasets revealed the integrated multimodal (IMM) model's superior performance over unimodal models. The IMM model achieved prediction accuracies of 0.86 in ADNI and 0.92 in BAI, surpassing unimodal models based solely on structural MRI (0.81 and 0.87) or plasma Aβ42/40 (0.73 and 0.81) predictors. Conclusions: Our IMM model, combining MRI and BBBM data, offers a highly accurate approach to predict brain amyloid PET positivity. This innovative multiplex biomarker strategy presents an accessible and cost-effective avenue for advancing Alzheimer's disease diagnostics, leveraging diverse pathologic features related to Aβ plaques and structural MRI.
MeSH term(s)	Humans ; Aged ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/pathology ; Plaque, Amyloid/diagnostic imaging ; Amyloid beta-Peptides ; Amyloid ; Positron-Emission Tomography ; Magnetic Resonance Imaging ; Biomarkers ; Cognitive Dysfunction/diagnostic imaging ; tau Proteins
Chemical Substances	Amyloid beta-Peptides ; Amyloid ; Biomarkers ; tau Proteins
Language	English
Publishing date	2024-04-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-231162
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Article ; Online: Does an Alzheimer's disease susceptibility gene influence the cognitive effects of cancer therapy?

Caselli, Richard J

Pediatric blood & cancer

2014 Volume 61, Issue 10, Page(s) 1739–1742

Abstract: The apolipoprotein E (APOE) e4 allele is the most prevalent genetic risk factor for Alzheimer's disease (AD). APOE e4 carriers suffer greater morbidity from head trauma, stroke, and carbon monoxide poisoning, yet possible interactions between APOE ... ...

Abstract	The apolipoprotein E (APOE) e4 allele is the most prevalent genetic risk factor for Alzheimer's disease (AD). APOE e4 carriers suffer greater morbidity from head trauma, stroke, and carbon monoxide poisoning, yet possible interactions between APOE genotype and cancer therapy on cognition are unclear. Neuropathological and biomarker studies of young asymptomatic APOE e4 carriers that show elevated neocortical amyloid and medial temporal neurofibrillary tangles and longitudinal neuropsychological studies that show accelerated memory decline beginning around age 55-60 years define preclinical AD and have set the stage for assessing the potential adverse cognitive effects of cancer therapy in APOE e4 carriers.
MeSH term(s)	Alzheimer Disease/genetics ; Antineoplastic Agents/adverse effects ; Apolipoprotein E4/genetics ; Cognition/drug effects ; Cognition/radiation effects ; Cranial Irradiation/adverse effects ; Genetic Predisposition to Disease/genetics ; Humans ; Neoplasms/therapy
Chemical Substances	Antineoplastic Agents ; Apolipoprotein E4
Language	English
Publishing date	2014-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2131448-2
ISSN	1545-5017 ; 1545-5009
ISSN (online)	1545-5017
ISSN	1545-5009
DOI	10.1002/pbc.24768
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Article ; Online: Age stratification corrects bias in estimated hazard of

Liu, Li / Caselli, Richard J

Alzheimer's & dementia (New York, N. Y.)

2018 Volume 4, Page(s) 602–608

Abstract: Introduction: The apolipoprotein E (APOE) e4 allele is a major genetic risk factor of late-onset Alzheimer's disease. However, its interaction with two other canonical risk factors, age and sex, is not clear. Previous studies have reported conflicting ... ...

Abstract	Introduction: The apolipoprotein E (APOE) e4 allele is a major genetic risk factor of late-onset Alzheimer's disease. However, its interaction with two other canonical risk factors, age and sex, is not clear. Previous studies have reported conflicting results on its differential effects in men and women, its association with young-onset AD before the age of 65 years, and its significance in genetic admixture populations. In these studies, the hazard of the e4 allele was assumed to be constant during aging. However, this hypothesis has not been tested and its violation may lead to significant biases and contribute to such discrepant findings. Methods: In a prospective cohort of 4727 subjects, we performed Cox regression analysis of the association of the e4 allele with AD age of onset. We then performed diagnostics on the resulting model and tested if the hazard of the e4 allele violated the assumption of proportionality during aging. We examined whether incorporating age stratifications and time-dependent coefficients could restore the proportionality. We then validated our findings in four independent cohorts. Results: Hazard of the e4 allele for AD was nonproportional. It took a stepwise decline around the age of 80 years for men and around the age of 75 years for women. By stratifying subjects into a younger group and an older group, we detected more consistent effects of the e4 allele across multiple independent cohorts. We also found that the e4 allele was a significant risk factor for young-onset AD with age of onset before 65 years. Discussion: Age compositions of study cohorts can significantly bias the estimated effect of the APOE genotype. Studies of AD should consider hidden age structures among subjects and routinely employ appropriate age and sex stratification strategies or nonparametric modeling in experimental designs and data analysis. Finally, we argue that the e4 allele is a risk factor not only for late-onset AD but also for young-onset AD.
Language	English
Publishing date	2018-10-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832891-7
ISSN	2352-8737 ; 2352-8737
ISSN (online)	2352-8737
ISSN	2352-8737
DOI	10.1016/j.trci.2018.09.006
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Article ; Online: An agnostic reevaluation of the amyloid cascade hypothesis of Alzheimer's disease pathogenesis: The role of APP homeostasis.

Caselli, Richard J / Knopman, David S / Bu, Guojun

Alzheimer's & dementia : the journal of the Alzheimer's Association

2020 Volume 16, Issue 11, Page(s) 1582–1590

Abstract: Objective: To reassess the role of amyloid beta (Aβ) and the amyloid precursor protein (APP) system in the pathogenesis of Alzheimer's disease (AD).: Background: APP is a cell adhesion molecule that has been highly conserved over the course of ... ...

Abstract	Objective: To reassess the role of amyloid beta (Aβ) and the amyloid precursor protein (APP) system in the pathogenesis of Alzheimer's disease (AD). Background: APP is a cell adhesion molecule that has been highly conserved over the course of phylogeny that has critical roles in brain development, synaptic plasticity, and the brain's intrinsic immune system. The amyloid cascade hypothesis describes a relatively linear, deterministic sequence of events triggered by a gain of Aβ peptide fragment toxicity that results in neurodegeneration and cognitive loss, yet well designed immunotherapy and beta secretase inhibitor trials that have successfully targeted Aβ have failed to have any consistent effects on the steady decline of cognition. New/updated hypothesis: Mutations of the APP and presenilin genes not only alter the ratio of longer to shorter Aβ fragments (resulting in a gain of Aβ toxicity), but also disrupt the normal homeostatic roles of their respective proteins. The evolutionary history, physiological importance, and complexity of the APP and presenilin systems, as well as other critical components including tau and apolipoprotein E (APOE) imply that altered function of such systems could have severe consequences that include but need not be limited to a gain of Aβ toxicity and would more generally result in altered homeostasis of APP-related functions. Major challenges addressed by our hypothesis: Challenges that a loss of APP homeostasis addresses better than the more limited gain of Aβ toxicity model include the topographic mismatches between Aβ and tau pathology, the profile and chronology of cognitive and biomarker changes that precede the clinical expression of mild cognitive impairment and dementia, and the disappointments of Aβ targeted therapeutics among others. Linkage to other major theories: The importance of APP, α- and β-secretases, the presenilins and γ-secretase, as well as tau was recognized by the authors of the amyloid cascade hypothesis, and has since led multiple investigators to propose alternative, more balanced hypotheses including reduced homeostasis and frank loss-of-function of key components that include but go beyond the currently envisioned linear model of Aβ toxicity.
MeSH term(s)	Alzheimer Disease ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Homeostasis ; Humans
Chemical Substances	Amyloid beta-Protein Precursor
Language	English
Publishing date	2020-06-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12124
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Article ; Online: The (Mis)diagnosis of Creutzfeldt-Jakob Disease.

Caselli, Richard J

Archives of neurology

2012 Volume 69, Issue 12, Page(s) 1554–1555

Language	English
Publishing date	2012-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	80049-1
ISSN	1538-3687 ; 0003-9942
ISSN (online)	1538-3687
ISSN	0003-9942
DOI	10.1001/2013.jamaneurol.1
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Article ; Online: Sex-Specific Multiparameter Blood Test for the Early Diagnosis of Alzheimer's Disease.

Cho, Hyung Joon / Schulz, Philip / Venkataraman, Lalitha / Caselli, Richard J / Sierks, Michael R

International journal of molecular sciences

2022 Volume 23, Issue 24

Abstract: Blood-based biomarkers are needed for the early diagnosis of Alzheimer's disease (AD). We analyzed longitudinal human plasma samples from AD and control cases to identify biomarkers for the early diagnosis of AD. Plasma samples were grouped based on ... ...

Abstract	Blood-based biomarkers are needed for the early diagnosis of Alzheimer's disease (AD). We analyzed longitudinal human plasma samples from AD and control cases to identify biomarkers for the early diagnosis of AD. Plasma samples were grouped based on clinical diagnosis at the time of collection: AD, mild cognitive impairment (MCI), and pre-symptomatic (preMCI). Samples were analyzed by ELISA using a panel of reagents against nine different AD-related amyloid-β (Aβ), tau, or TDP-43 variants. Receiver operating characteristic (ROC) curves of different biomarker panels for different diagnostic sample groups were determined. Analysis of all of the samples gave a sensitivity of 92% and specificity of 76% for the diagnosis of AD. Early-stage diagnosis of AD, utilizing only the preMCI and MCI samples, identified 88% of AD cases. Using sex-biased biomarker panels, early diagnosis of AD cases improved to 96%. Using the sex-biased panels, we also identified 6 of the 25 control group cases as being at high risk of AD, which is consistent with what is expected given the advanced age of the control cases. Specific AD-associated protein variants are effective blood-based biomarkers for the early diagnosis of AD. Notably, significant differences were observed in biomarker profiles for the early detection of male and female AD cases.
MeSH term(s)	Male ; Female ; Humans ; Alzheimer Disease ; tau Proteins ; Amyloid beta-Peptides ; Cognitive Dysfunction/diagnosis ; Early Diagnosis ; Hematologic Tests ; Biomarkers ; Peptide Fragments
Chemical Substances	tau Proteins ; Amyloid beta-Peptides ; Biomarkers ; Peptide Fragments
Language	English
Publishing date	2022-12-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232415670
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Article ; Online: Hippocampal connectivity and memory decline in cognitively intact APOE ε4 carriers.

Baxter, Leslie C / Limback-Stokin, Martin / Patten, K Jakob / Arreola, Alejandra Cabello / Locke, Dona E C / Hu, Leland / Zhou, Yuxiang / Caselli, Richard J

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 9, Page(s) 3806–3814

Abstract: Introduction: Resting-state functional magnetic resonance imaging (fMRI) graph theory may help detect subtle functional connectivity changes affecting memory prior to impairment.: Methods: Cognitively normal apolipoprotein E (APOE) ε4 carriers/ ... ...

Abstract	Introduction: Resting-state functional magnetic resonance imaging (fMRI) graph theory may help detect subtle functional connectivity changes affecting memory prior to impairment. Methods: Cognitively normal apolipoprotein E (APOE) ε4 carriers/noncarriers underwent longitudinal cognitive assessment and one-time MRI. The relationship of left/right hippocampal connectivity and memory trajectory were compared between carriers/noncarriers. Results: Steepness of verbal memory decline correlated with decreased connectivity in the left hippocampus, only among APOE ε4 carriers. Right hippocampal metrics were not correlated with memory and there were no significant correlations in the noncarriers. Verbal memory decline correlated with left hippocampal volume loss for both carriers and noncarriers, with no other significant volumetric findings. Discussion: Findings support early hippocampal dysfunction in intact carriers, the AD disconnection hypothesis, and left hippocampal dysfunction earlier than the right. Combining lateralized graph theoretical metrics with a sensitive measure of memory trajectory allowed for detection of early-stage changes in APOE ε4 carriers before symptoms of mild cognitive impairment are present. Highlights: Graph theory connectivity detects preclinical hippocampal changes in APOE ε4 carriers. The AD disconnection hypothesis was supported in unimpaired APOE ε4 carriers. Hippocampal dysfunction starts asymmetrically on the left.
MeSH term(s)	Humans ; Apolipoprotein E4/genetics ; Heterozygote ; Hippocampus/pathology ; Memory ; Memory Disorders/diagnostic imaging ; Memory Disorders/genetics ; Magnetic Resonance Imaging ; Alzheimer Disease/pathology ; Neuropsychological Tests
Chemical Substances	Apolipoprotein E4
Language	English
Publishing date	2023-03-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13023
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Article ; Online: Phenotypic differences between apolipoprotein E genetic subgroups: research and clinical implications.

Caselli, Richard J

Alzheimer's research & therapy

2012 Volume 4, Issue 3, Page(s) 20

Abstract: With the recent interest in Alzheimer's disease course modification and earlier, even preclinical, intervention, questions have arisen regarding the potentially confounding impact of apolipoprotein E (APOE) genotype on study design, therapeutic outcomes, ...

Abstract	With the recent interest in Alzheimer's disease course modification and earlier, even preclinical, intervention, questions have arisen regarding the potentially confounding impact of apolipoprotein E (APOE) genotype on study design, therapeutic outcomes, and even clinical practice. APOE e4 carriers have a faster rate of cognitive decline both preclinically and during the mild cognitive impairment (MCI) stage, and a higher burden of cerebrovascular amyloid that may be the basis for the observed gene-dose-related increased frequency of immunomodulatory therapy-induced meningoencephalitis and cerebral microhemorrhages. To date, this has impacted study design in some research trials but not clinical practice.
Language	English
Publishing date	2012-06-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/alzrt123
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