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Lowe, V. J.

Publications and source records attributed to Lowe, V. J..

5 recordsLinked to original sources

A shared slowing axis and phenotype-specific rhythms link clinical EEG to FDG-PET dementia phenotypes

Early and accurate identification of neurodegenerative disorders has notable implications for treatment and quality of life. Whereas neuroimaging-based biomarkers can accurately identify neurodegenerative subtypes, EEG represents a low-cost alternative that could expand access to dementia care. Here, we investigated whether six data-driven EEG latent factors, derived by nonnegative tensor decomposition of clinical EEGs, differ systematically across FDG-PET-defined neurodegenerative phenotypes. In 455 patients with EEG and FDG-PET acquired within one year of each other, factor expression was compared across 14 diagnostic classes assigned by StateViewer, a validated artificial intelligence framework for FDG-PET interpretation. To separate disease-general severity from phenotype-specific topography, each factor was also regressed on a subject-level slowing index. Finally, we related the factors to regional FDG uptake and to neuropsychological performance (n = 98) and assessed their potential utility for single-subject classification. Four factors reflecting neurophysiological oscillations (posterior alpha, Rolandic beta, frontotemporal delta-theta and posterior theta-slow alpha) varied significantly across phenotypes, with attenuation of faster and augmentation of slower rhythms most pronounced in dementia with Lewy bodies (DLB), dysexecutive Alzheimer disease (AD) and posterior cortical atrophy, whereas factors dominated by eye-movement and muscle artifact showed no robust phenotypic association. Alpha and beta effects were largely attributable to overall slowing, whereas posterior theta-slow alpha became more phenotype-specific after adjustment (eta-squared 0.082 to 0.147), dissociating the Alzheimer disease spectrum from frontotemporal syndromes. The slowing index tracked with an FDG-PET pattern highly associated with DLB across the cohort, irrespective of assigned phenotype (r = 0.51, P < 0.001). Consistent with a model in which dementia phenotypes reflect altered hippocampal-neocortical oscillatory coupling (stochastic latent oscillatory diffusion), frontotemporal delta-theta tracked a limbocortical axis of metabolic pattern expression, rising with neocortical and falling with limbic-predominant involvement, independent of overall slowing and phenotype. Each factor mapped onto a distinct metabolic topography, with frontotemporal delta-theta resembling Alzheimer-type hypometabolism and posterior theta-slow alpha the medial occipital hypometabolism of DLB. In terms of neuropsychological performance, Rolandic beta was associated with executive functions, and frontotemporal delta-theta with memory, visuospatial and global performance. Using these four factors alone, an exploratory logistic regression classifier separated cognitively unimpaired participants from DLB, posterior cortical atrophy, typical AD, and dysexecutive AD (area under the curve > 0.8) but poorly discriminated frontotemporal dementia phenotypes canonically associated with 4-repeat tau. Thus, data-driven decomposition of clinical EEG separates oscillatory activity from artifact into factors that track metabolic phenotype, regional metabolism and cognition, capturing both overall slowing and phenotype-specific patterns. This work informs the further development of scalable, biology-informed EEG-based phenotyping of neurodegenerative disease.

neuroscience↗

Disruptions in glucose and amyloid-beta transport in mouse models manifesting metabolic syndrome

Studies in humans and murine models have pointed towards a possible link between metabolic syndrome, which shows insulin resistance and metabolic dysregulation, and Alzheimer's disease (AD) pathology marked by amyloid-beta (A{beta}) accumulation and hypometabolism in the brain. Yet, the underlying biological mechanisms by which metabolic syndrome affects these pathological changes in AD brain remain unknown. We hypothesized that insulin resistance is responsible for alterations in blood-brain barrier (BBB) transport of A{beta} peptides and glucose. This hypothesis was tested by employing radiolabeled ligands (125I-A{beta}40, 125I-A{beta}42, and 18F-FDG) in high-fat diet (HFD)-fed mouse models that manifest metabolic syndrome. Further, we assessed alterations in the expression of various molecular mediators within the brain microcapillaries harvested from both low-fat diet (LFD)-fed and HFD-fed mice. Our findings show that HFD-fed mice developed peripheral insulin resistance and obesity. In addition, HFD-fed mice demonstrated an increase in the influx rate of A{beta} peptides and a reduction in 18F-FDG (a glucose surrogate) influx rate compared to LFD-fed mice. These transport changes are associated with the increase in the BBB endothelial expression of RAGE (receptor to traffic A{beta} from plasma-to-brain) and reduction of GLUT1 (glucose transporter) expression in HFD-fed mice compared to LFD-fed mice. Moreover, disruption in insulin signaling, as indicated by reduced pAKT and pERK expression, was observed in HFD-fed mice. Inhibiting AKT or ERK phosphorylation resulted in similar changes in A{beta} and glucose uptake in polarized BBB endothelial cell monolayers in vitro. These results indicate that high-fat diet induced metabolic syndrome may lead to BBB dysfunction, characterized by increased plasma-to-brain A{beta} trafficking and diminished glucose transport at the BBB, thereby aggravating the expression of AD pathological hallmarks.

neuroscience↗

Amyloid Beta Peptides Inhibit Glucose Transport at the Blood-brain Barrier by Disrupting Insulin-Akt Pathway in Alzheimer's Disease

Disruptions in glucose uptake and metabolism in the brain are implicated in metabolic disorders and Alzheimers disease (AD). Toxic soluble amyloid-beta (sA{beta}) peptides accumulating in the brain and plasma of AD patients were suggested to promote blood-brain barrier (BBB) dysfunction, brain hypometabolism, and cognitive decline. Exposure to sA{beta} peptides is reported to interfere with glucose metabolism in the brain parenchyma, although their effects on the BBB have not been fully characterized. Our data showed that the brain uptake of glucose surrogate, [18F]-fluorodeoxyglucose (18FDG), was reduced significantly in APP/PS1 transgenic mice (overproduce A{beta}) compared to wild-type (WT) mice. In addition, the influx rate of 18FDG was also decreased in both A{beta}40 and A{beta}42 pre-infused mice compared to control mice. Glucose is primarily delivered from blood into the brain via glucose transporter 1 (GLUT1). The confocal microscopy experiment showed that A{beta}40 and A{beta}42 peptides significantly decreased GLUT1 expression in polarized human cerebral microvascular endothelial cell (hCMEC/D3) monolayers. Insulin-AKT pathway has been observed to induce glucose uptake via regulating the expression of TXNIP, the only -arrestin protein known to bind to thioredoxin. We found that A{beta}40 and A{beta}42 peptides decreased p-AKT and increased TXNIP expression in the hCMEC/D3 cell monolayers. MK2206, a kinase inhibitor of AKT, was used to confirm that inhibition of insulin/AKT pathway reduced GLUT1 expression in an insulin-independent manner in the hCMEC/D3 cell monolayers. These results suggest that inhibitory effects of sA{beta} on GLUT1 expression are mediated by inhibition of the insulin/AKT pathway. The role of TXNIP on endothelial GLUT1 expression was investigated using resveratrol, which has been reported to downregulate TXNIP overexpression. Consistently, resveratrol treatment led to a significant increase in GLUT1 expression in the hCMEC/D3 cell monolayers. Furthermore, by co-incubation of resveratrol and sA{beta} peptides in hCMEC/D3 cell monolayers, we found that resveratrol rectified the aberrant TXNIP expression caused by sA{beta} peptides. Together, these findings provide novel evidence that toxic sA{beta} peptide exposure inhibits glucose transport at the BBB by decreasing GLUT1 expression via the insulin/Akt/TXNIP axis.

pharmacology and toxicology↗

Deconvolution of plasma pharmacokinetics from dynamic heart imaging data obtained by SPECT/CT imaging

Plasma pharmacokinetic (PK) data is required as an input function for graphical analysis (e.g., Patlak plot) of single positron emission computed tomography/computed tomography (SPECT/CT) and positron emission tomography/CT (PET/CT) data to evaluate tissue influx rate of radiotracers. Dynamic heart imaging data is often used as a surrogate of plasma PK. However, accumulation of radiolabel (representing both intact and degraded tracer) in the heart tissue may interfere with accurate prediction of plasma PK from the heart data. Therefore, we developed a compartmental model, which involves forcing functions to describe intact and degraded radiolabeled proteins in plasma and their accumulation in heart tissue, to deconvolve plasma PK of 125I-amyloid beta 40 (125I-A{beta}40) and 125I-insulin from their dynamic heart imaging data. The three-compartment model was shown to adequately describe the plasma concentration-time profile of intact/degraded proteins and the heart radioactivity time data obtained from SPECT/CT imaging for both tracers. The model was successfully applied to deconvolve the plasma PK of both tracers from their naive datasets of dynamic heart imaging. In agreement with our previous observations made by conventional serial plasma sampling, the deconvolved plasma PK of 125I-A{beta}40 and 125I-insulin in young mice exhibited lower area under the curve (AUC) than the aged mice. Further, Patlak plot parameters (Ki) extracted using deconvolved plasma PK as input function successfully recapitulated age-dependent blood-to-brain influx kinetics changes for both 125I-A{beta}40 and 125I-insulin. Therefore, the compartment model developed in this study provides a novel approach to deconvolve plasma PK of radiotracers from their noninvasive dynamic heart imaging. This method facilitates the application of preclinical SPECT or PET imaging data to characterize distribution kinetics of tracers where simultaneous plasma sampling is not feasible.

pharmacology and toxicology↗

Synthesizing Images of Tau Pathology from Cross-modal Neuroimaging using Deep Learning

Given the prevalence of dementia and the development of pathology-specific disease modifying therapies, high-value biomarker strategies to inform medical decision making are critical. In-vivo tau positron emission tomography (PET) is an ideal target as a biomarker for Alzheimers disease diagnosis and treatment outcome measure. However, tau PET is not currently widely accessible to patients compared to other neuroimaging methods. In this study, we present a convolutional neural network (CNN) model that impute tau PET images from more widely-available cross-modality imaging inputs. Participants (n=1,192) with brain MRI, fluorodeoxyglucose (FDG) PET, amyloid PET, and tau PET were included. We found that a CNN model can impute tau PET images with high accuracy, the highest being for the FDG-based model followed by amyloid PET and MRI. In testing implications of AI-imputed tau PET, only the FDG-based model showed a significant improvement of performance in classifying tau positivity and diagnostic groups compared to the original input data, suggesting that application of the model could enhance the utility of the metabolic images. The interpretability experiment revealed that the FDG- and MRI-based models utilized the non-local input from physically remote ROIs to estimate the tau PET, but this was not the case for the PiB-based model. This implies that the model can learn the distinct biological relationship between FDG PET, MRI, and tau PET from the relationship between amyloid PET and tau PET. Our study suggests that extending neuroimagings use with artificial intelligence to predict protein specific pathologies has great potential to inform emerging care models.

bioengineering↗