Sex and APOE4-specific links between cardiometabolic risk factors and white matter alterations in individuals with a family history of Alzheimer's disease.

Early detection of pathological changes in Alzheimer's disease (AD) has garnered significant attention in the last few decades as interventions aiming to prevent progression will likely be most effective when initiated early. White matter (WM) alterations are among the earliest changes in AD, yet limited work has comprehensively characterized the effects of AD risk factors on WM. In older adults with a family history of AD, we investigated the sex-specific and APOE genotype-related relationships between WM microstructure and risk factors.

A novel method for harmonization of PET image spatial resolution without phantoms.

Background: Estimation of the spatial resolution in real images is extremely important in several fields, including crystallography, optics, microscopy, and tomography. In human PET imaging, estimating spatial resolution typically involves the acquisition of images from a physical phantom, typically a Hoffman phantom, which poses a logistical burden, especially in large multi-center studies. Indeed, phantom images may not always be readily available, and this method requires constant monitoring of scanner updates or replacements, scanning protocol changes, and image reconstruction guidelines to establish a equivalence with scans acquired from human subjects.

Tau-related reduction of glucose metabolism in mild cognitive impairment occurs independently of APOE ε4 genotype and is influenced by Aβ.

Introduction: Positron emission tomography (PET) imaging studies have shown that amyloid beta (Aβ) is significantly correlated with glucose metabolism in mild cognitive impairment independently of the apolipoprotein E (APOE) ε4 genotype.

Methods: We used a singular value decomposition (SVD) approach to pairwise cross-correlation among tau, Aβ, and fluorodeoxyglucose PET images. The resulting SVD-based tau and Aβ scores as well as the APOE ε4 genotype, were entered as predictors in a voxelwise general linear model for statistical assessment of their effect on FDG.

Patient-centered brain transcriptomic and multimodal imaging determinants of clinical progression, physical activity, and treatment needs in Parkinson's disease.

We continue to lack a clear understanding on how the biological and clinical complexity of Parkinson's disease emerges from molecular to macroscopic brain interactions. Here, we use personalized multiscale spatiotemporal computational brain models to characterize for the first time the synergistic links between genes, several multimodal neuroimaging-derived biological factors, clinical profiles, and therapeutic needs in PD. We identified genes modulating PD-caused brain reorganization in dopamine transporter level, neuronal activity integrity, microstructure, dendrite density and tissue atrophy.

In-vivo neuronal dysfunction by Aβ and tau overlaps with brain-wide inflammatory mechanisms in Alzheimer's disease.

The molecular mechanisms underlying neuronal dysfunction in Alzheimer's disease (AD) remain uncharacterized. Here, we identify genes, molecular pathways and cellular components associated with whole-brain dysregulation caused by amyloid-beta (Aβ) and tau deposits in the living human brain. We obtained resting-state functional MRI (rs-fMRI), Aβ- and tau-PET for 47 cognitively unimpaired and 16 AD participants from the Translational Biomarkers in Aging and Dementia cohort.