Biology subjects

Buxton, O. M.

Publications and source records attributed to Buxton, O. M..

3 recordsLinked to original sources

bioRxiv2025

Lower slow wave sleep and rapid eye-movement sleep are associated with brain atrophy of AD-vulnerable regions

Study objectivesSleep deficiency is associated with Alzheimers disease (AD) pathogenesis. We examined the association of sleep architecture with anatomical features observed in AD: (1) atrophy of hippocampus, entorhinal, inferior parietal, parahippocampal, precuneus, and cuneus regions ("AD-vulnerable regions") and (2) cerebral microbleeds. MethodsIn 271 participants of the Atherosclerosis Risk in the Communities Study, we examined the association of baseline sleep architecture with anatomical features identified on brain MRI 13[~]17 years later. Sleep architecture was quantified as the proportion of slow wave sleep (SWS), proportion of rapid eye-movement sleep (REM), and arousals index using polysomnography. Outcomes included (1) volumetric measurements of each AD-vulnerable region and (2) the presence of any cerebral microbleeds (CMBs) and that of lobar CMBs, which are more specifically associated with AD. We analyzed the association of each sleep predictor with each MRI outcome, adjusting for covariates. ResultsHaving less SWS was associated with smaller inferior parietal region ({beta}=-44.19 mm3 [95%CI=-76.63,-11.76]) and cuneus ({beta}=-11.99 mm3 [-20.93,-3.04]) after covariate adjustment. Having less REM was associated with smaller inferior parietal region ({beta}=-75.52 mm3 [-129.34, -21.70]) and precuneus ({beta}=-31.93 mm3 [-63.79,-0.07]). After FDR adjustments, lower SWS and REM, respectively, were associated with smaller inferior parietal region. Arousal index was not associated with the volumes of AD-vulnerable regions. None of the sleep architecture variables were associated with CMBs or lobar CMBs. ConclusionsSleep deficiency is associated with the atrophy of the inferior parietal region, which is observed in early AD. Sleep architecture may be a modifiable risk factor for AD. Brief summarya. Current Knowledge/Study Rationale: two sentences summarizing why the study was doneWhile impaired sleep architecture has been associated with Alzheimers disease [AD] diagnosis and cognitive decline. To better understand the impact of sleep on AD pathogenesis, this study examined the association of sleep architecture with anatomical features observed in AD, including the atrophy of AD-vulnerable regions and CMBs. b. Study Impact: two sentences summarizing how the study impacts the fieldOur study shows that lower slow wave sleep and rapid eye movement sleep may be precipitating factors of inferior parietal region atrophy, which is associated with AD risk. Importantly, the current studys findings can help characterize underlying mechanisms of how sleep deficiency, a prevalent disturbance among middle-aged and older adults, may facilitate AD pathogenesis and cognitive impairment.

neuroscience↗

bioRxiv2022

An orderly sequence of autonomic and neural events at transient arousal changes

Resting-state functional magnetic resonance imaging (rsfMRI) allows the study of functional brain connectivity based on spatially structured variations in neuronal activity. Proper evaluation of connectivity requires removal of non-neural contributions to the fMRI signal, in particular hemodynamic changes associated with autonomic variability. Regression analysis based on autonomic indicator signals has been used for this purpose, but may be inadequate if neuronal and autonomic activity covary. To investigate this potential co-variation, we performed rsfMRI experiments while concurrently acquiring electroencephalography and autonomic indicator signals, including heart rate, respiratory depth, and peripheral vascular tone. We identified a recurrent and systematic pattern of fMRI, EEG, and autonomic changes coincidental with intermittent arousal, suggesting arousal modulation. The temporal relationship between the various signals indicated combined neural and autonomic contribution to the fMRI signal, both of which involve widespread brain areas. The fMRI changes included brief signal reductions in salience and default-mode networks, and the thalamus, followed by a biphasic global change. These results suggest that proper measurement of functional connectivity with fMRI requires accounting for the full spectrum of autonomic and neural changes, as well as their co-variation during arousal state transitions.

neuroscience↗

bioRxiv2020

The coupling of global brain activity and cerebrospinal fluid inflow is correlated with Alzheimer's disease related pathology

The glymphatic system plays an important role in clearing the amyloid-{beta} and tau proteins that are closely linked to Alzheimers disease (AD) pathology. Glymphatic clearance, as well as amyloid-{beta} accumulation, is highly dependent on sleep, but the sleep-dependent driving forces behind cerebrospinal fluid (CSF) movements essential to the glymphatic flux remain largely unclear. Recent studies have reported that widespread, high-amplitude spontaneous brain activations in the drowsy state and during sleep, which are shown as large global signal peaks in resting-state fMRI, is coupled with the CSF movements, suggesting their potential link to the glymphatic flux and metabolite clearance. By analyzing multimodal data from the Alzheimers Disease Neuroimaging Initiative project, here we showed that the coupling between the global fMRI signal and CSF influx is correlated with AD-related pathology, including various risk factors for AD, the severity of AD-related diseases, the cortical amyloid-{beta} level, and the cognitive decline over a two-year follow-up. These results provide critical initial evidence for involvement of sleep-dependent global brain activity, as well as the associated physiological modulations, in the clearance of AD-related brain waste.

neuroscience↗