No abstract

Mindfulness meditation has been shown to be beneficial for a range of different health conditions, impacts brain function and structure relatively quickly, and has shown promise with aging samples. Functional magnetic resonance imaging metrics provide insight into neurovascular health which plays a key role in both normal and pathological aging processes. Experimental mindfulness meditation studies that included functional magnetic resonance metrics as an outcome measure may point to potential neurovascular mechanisms of action relevant for aging adults that have not yet been previously examined. We first review the resting-state magnetic resonance studies conducted in exclusively older adult age samples. Findings from older adult-only samples are then used to frame the findings of task magnetic resonance imaging studies conducted in both clinical and healthy adult samples. Based on the resting-state studies in older adults and the task magnetic resonance studies in adult samples, we propose three potential mechanisms by which mindfulness meditation may offer a neurovascular therapeutic benefit for older adults: (1) a direct neurovascular mechanism via increased resting-state cerebral blood flow; (2) an indirect anti-neuroinflammatory mechanism via increased functional connectivity within the default mode network, and (3) a top-down control mechanism that likely reflects both a direct and an indirect neurovascular pathway.

Background: There are now clinically available automated MRI analysis software programs that compare brain volumes of patients to a normative sample and provide z-score data for various brain regions. These programs have yet to be validated in primary progressive aphasia (PPA). Objective: To address this gap in the literature, we examined Neuroreadertrademark z-scores in PPA, relative to visual MRI assessment. We predicted that Neuroreadertrademark 1) would be more sensitive for detecting left >  right atrophy in the cortical lobar regions in logopenic variant PPA clinical phenotype (lvPPA), and 2) would distinguish lvPPA (n = 11) from amnestic mild cognitive impairment (aMCI; n = 12). Methods: lvPPA or aMCI patients who underwent MRI with Neuroreadertrademark were included in this study. Two neuroradiologists rated 10 regions. Neuroreadertrademark lobar z-scores for those 10 regions, as well as a hippocampal asymmetry metric, were included in analyses. Results: Cohen’s Kappa coefficients were significant in 10 of the 28 computations (k = 0.351 to 0.593, p≤0.029). Neuroradiologists agreed 0% of the time that left asymmetry was present across regions. No significant differences emerged between aMCI and lvPPA in Neuroreadertrademark z-scores across left or right frontal, temporal, or parietal regions (ps >  0.10). There were significantly lower z-scores in the left compared to right for the hippocampus, as well as parietal, occipital, and temporal cortices in lvPPA. Conclusion: Overall, our results indicated moderate to low interrater reliability, and raters never agreed that left asymmetry was present. While lower z-scores in the left hemisphere regions emerged in lvPPA, Neuroreadertrademark failed to differentiate lvPPA from aMCI.

Patients suffering from long COVID report cognitive symptoms months after disease onset, which may be related to neurovascular changes. Here, we evaluated functional connectivity in long COVID elderly patients and control subjects using a region of lower cerebrovascular reactivity (CVR) as the seed. We found significantly lower connectivity in long COVID patients that was widespread potentially linking alterations in CVR to functional connectivity and reduced cognitive ability in long COVID patients.