Olfactory adaptation, the progressive reduction of neural responses to repeated odor stimulation, is closely linked to cognitive function and is altered in Alzheimer's disease (AD). However, its evolution across biomarker-defined stages and relationship with plasma p-tau217 remain unclear. We studied 168 participants classified by plasma p-tau217: cognitively normal (p-tau217-NC, n = 37; p-tau217+NC, n = 8), subjective cognitive decline (p-tau217-SCD, n = 57; p-tau217+SCD, n = 16), and mild cognitive impairment (p-tau217-MCI, n = 40; p-tau217+MCI, n = 10). Odor-induced fMRI with four concentrations (0.032%, 0.1%, 0.32%, 1.0%) presented in a fixed ascending order, although concentration effects could not be fully separated from time-related factors and other confounders, to assess activation in the primary olfactory cortex (POC), hippocampus (HP), and parietal lobe (PL). Receiver operating characteristic (ROC) analyses were performed using logistic regression models. In NC groups, adaptation emerged at 0.1% and 0.32% odor conditions. In p-tau217-SCD, POC adaptation was delayed to 1.0% odor condition, HP was largely preserved, and PL was dysregulated. p-tau217+SCD and MCI groups showed delayed and dysregulated adaptation across all regions. Odor adptations were associated with plasma p-tau217 levels and olfactory memory (p_unc < 0.05, p_FDR > 0.05). Furthermore, plasma p-tau217 partially mediated the relationship between adaptation-related alterations and olfactory memory. ROC analyses indicated that olfactory adaptation may distinguished individuals across disease stages, require further confirmation in independent cohorts. These findings reveal that impaired olfactory adaptation may represent an early signature associated with AD continuum, particularly in SCD and p-tau217-positive stages.
Xi Wu, Yajing Zhu, Shunshun Du et al.· NeuroImage· 0 citations
AIMS
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly linked to cognitive decline, yet the hepatic factors associated with imaging-derived neurovascular coupling (NVC) remain unclear. This study aimed to investigate whether liver stiffness or liver fat content was more closely associated with resting-state CBF-ReHo surrogate measures.
MATERIALS AND METHODS
A total of 130 participants including 98 MASLD patients and 32 age- and education-matched healthy controls (HCs) underwent clinical assessment, neuropsychological testing, and multi-modal MRI. Liver stiffness and fat content were quantified using MR elastography (MRE) and MRI-proton density fat fraction (PDFF). Imaging-derived NVC was assessed using global cerebral blood flow (CBF)-regional homogeneity (ReHo) coupling and voxel-wise CBF/ReHo ratios, interpreted as resting-state surrogates rather than direct stimulus-evoked NVC. Multivariable regression and exploratory mediation analyses were employed.
RESULTS
Compared to HCs and patients with lower liver stiffness (MASLD_low), those with higher liver stiffness (MASLD_high) showed reduced global CBF-ReHo coupling and altered CBF/ReHo ratios, primarily localized to the bilateral superior temporal pole/superior temporal gyrus (TPOsup). In multivariable regression, liver stiffness remained independently associated with TPOsup CBF/ReHo ratios (p < 0.001). Exploratory mediation analysis showed a statistically significant indirect association between hepatocellular injury markers and TPOsup CBF/ReHo ratios involving MRE-derived liver stiffness (95% CI: 0.0795-0.2790).
CONCLUSIONS
Within this cohort and the observed PDFF range, MRE-derived liver stiffness was more closely associated with imaging-derived NVC surrogate measures than liver fat content in MASLD. These findings are hypothesis-generating and require validation in longitudinal studies.
Zhuoru Jiang, Futao Chen, Hailong Zhang et al.· Diabetes, obesity and metabo...· 0 citations
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