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We tested whether chronic supplementation with resveratrol (a phytoestrogen) could improve cerebrovascular function, cognition and mood in post-menopausal women. Eighty post-menopausal women aged 45–85 years were randomised to take trans-resveratrol or placebo for 14 weeks and the effects on cognitive performance, cerebral blood flow velocity and pulsatility index (a measure of arterial stiffness) in the middle cerebral artery (using transcranial Doppler ultrasound), and cerebrovascular responsiveness (CVR) to both cognitive testing and hypercapnia were assessed. Mood questionnaires were also administered. Compared to placebo, resveratrol elicited 17% increases in CVR to both hypercapnic (p = 0.010) and cognitive stimuli (p = 0.002). Significant improvements were observed in the performance of cognitive tasks in the domain of verbal memory (p = 0.041) and in overall cognitive performance (p = 0.020), which correlated with the increase in CVR (r = 0.327; p = 0.048). Mood tended to improve in multiple measures, although not significantly. These results indicate that regular consumption of a modest dose of resveratrol can enhance both cerebrovascular function and cognition in post-menopausal women, potentially reducing their heightened risk of accelerated cognitive decline and offering a promising therapeutic treatment for menopause-related cognitive decline.

Menopause marks a major milestone in female reproductive ageing. It is characterized by the cessation of ovarian function and a concomitant decline in hormones such as oestradiol. Subsequently, females undergoing menopausal transition experience a progressive increase in cardiovascular and cerebrovascular disease risk. During menopause, reductions in nitric oxide (NO) bioavailability, endothelial dysfunction, increases in systemic inflammation, oxidative stress, and impaired vascular remodelling may contribute towards an accelerated decline in the function of cerebral and peripheral vascular systems. Historically, hormone therapy (HT) has been used as a means of managing vascular disease risk and reducing menopause‐associated vasomotor symptoms such as hot flushes, though some studies suggest regular exercise has the potential to be a promising alternative. Regular aerobic exercise during early postmenopause may slow vascular decline by improving NO and oestradiol bioavailability, promoting positive vascular remodelling and lowering systemic inflammation. However, exercise‐mediated improvements in markers of vascular function are not consistently observed in oestradiol‐deficient postmenopausal women. Emerging evidence suggests that due to the greater oestradiol bioavailability during early postmenopause, vascular adaptations to exercise may be enhanced during this stage, as opposed to late postmenopause. Subsequently it may be important to begin regular exercise in the years preceding and immediately following the final menstrual period to slow the progression of vascular disease risk during perimenopause and beyond. The present review will provide a summary of our current understanding of how vascular function is affected during menopause and the role of regular aerobic and resistance exercise training in managing vascular disease risk. What is the topic of this review? This review focuses on the physiological changes that contribute to the accelerated risk of vascular disease throughout stages of menopause and the role that exercise may play in managing this risk. What advances does it highlight? This review acts as a summary of our current understanding of the therapeutic role of exercise throughout menopause and how it may contribute to both the management and the preservation of vascular health.

To test the hypothesis that hot water immersion (HWI) improves cerebrovascular function via shear‐mediated mechanisms, this study determined cerebrovascular reactivity to carbon dioxide () before and after 60 min of 39°C HWI and a 21°C air control (CON) in 15 healthy participants. Thermal and haemodynamic variables were assessed throughout the trials, and was determined by a 4‐min inhalation of hypercapnic gas (6% CO 2 , 21% O 2 , N 2 balance) and the assessment of internal carotid artery (ICA) blood flow by duplex ultrasound before and 45 min after HWI and CON. At 60 min of the interventions, core body temperature (CON, 36.9 ± 0.3°C; HWI, 38.1 ± 0.3°C, P  < 0.01), heart rate ( P  < 0.01) and ICA conductance ( P  < 0.01) were higher in HWI than CON, while, mean arterial blood pressure was lower (CON, 82 ± 9 mmHg; HWI 65 ± 8 mmHg, P  < 0.01). No differences were observed for ICA diameter, ICA blood velocity, ICA shear rate and ICA blood flow between HWI and CON (all P  > 0.05). ICA did not change after either CON (pre: 13.9 ± 9.2 to post: 11.3 ± 6.1 mL min −1  mmHg −1 ) or HWI (pre: 14.6 ± 7.9 to post: 10.9 ± 5.4 mL min −1  mmHg −1 ; Interaction P  = 0.65). In conclusion, HWI reduced blood pressure and increased ICA conductance (i.e. autoregulation) to maintain blood flow to the brain; however, HWI did not influence subsequent cerebrovascular function, as assessed by . What is the central question of this study? Does a single session of whole‐body hot water immersion increase internal carotid artery blood flow and shear rate, and transiently increase subsequent cerebrovascular function, assessed by volumetric cerebrovascular reactivity to hypercapnia? What is the main finding and its importance? Whole‐body hot water immersion decreased blood pressure and increased internal carotid artery cerebrovascular conductance but not volumetric blood flow or shear rate. Subsequent cerebrovascular reactivity remained unaltered following hot water immersion, indicating no acute influence of heating on volumetrically assessed cerebrovascular function.

Research has suggested a number of beneficial effects arising from the consumption of dietary flavonoids, found in foods such as cocoa, apples, tea, citrus fruits and berries on cardiovascular risk factors such as high blood pressure and endothelial dysfunction. These effects are thought to have a significant impact upon both vascular and cerebrovascular health, ultimately with the potential to prevent cardiovascular and potentially neurodegenerative disease with a vascular component, for example vascular dementia. This review explores the current evidence for the effects of flavonoid supplementation on human endothelial function and both peripheral and cerebral blood flow (CBF). Evidence presented includes their potential to reduce blood pressure in hypertensive individuals, as well as increasing peripheral blood perfusion and promoting CBF in both healthy and at-risk populations. However, there is great variation in the literature due to the heterogeneous nature of the randomised controlled trials conducted. As such, there is a clear need for further research and understanding within this area in order to maximise potential health benefits.

We compared the differences in cerebrovascular and cognitive function between 13 aerobic exercise trained, older adults and 13 age-, height- and sex-matched sedentary, untrained controls. We determined whether other measures accounted for differences in cerebrovascular and cognitive function between these groups and examined the associations between these functions. Participants undertook anthropometric, mood, cardiovascular, exercise performance, strength, cerebrovascular, and cognitive measurements, and a blood collection. Transcranial Doppler ultrasonography determined cerebrovascular responsiveness (CVR) to hypercapnia and cognitive stimuli. The trained group had a higher CVR to hypercapnia (80.3 ± 7.2 vs 35.1 ± 6.7%, P < 0.001), CVR to cognitive stimuli (30.1 ± 2.9 vs 17.8 ± 1.4%, P = 0.001) and total composite cognitive score (117 ± 2 vs 98 ± 4, P < 0.001) than the controls. These parameters no longer remained statistically different between the groups following adjustments for covariates. There were positive correlations between the total composite cognitive score and CVR to hypercapnia (r = 0.474, P = 0.014) and CVR to cognitive stimuli (r = 0.685, P < 0.001). We observed a relationship between cerebrovascular and cognitive function in older adults and an interaction between regular lifelong aerobic exercise training and cardiometabolic factors that may directly influence these functions.

Deficits in the cerebral microcirculation contribute to age-related cognitive decline. In a pilot study of postmenopausal women, we found that supplementation with a low dose of resveratrol, a phytoestrogen, for 14 weeks improved cerebrovascular and cognitive functions. We have since undertaken a larger, longer term study to confirm these benefits. Postmenopausal women aged 45–85 years (n = 129) were randomized to take placebo or 75 mg trans-resveratrol twice daily for 12 months. Effects on cognition, cerebral blood flow, cerebrovascular responsiveness (CVR) and cardiometabolic markers (blood pressure, diabetes markers and fasting lipids) were assessed. Compared to placebo, resveratrol improved overall cognitive performance (P < 0.001) and attenuated the decline in CVR to cognitive stimuli (P = 0.038). The latter effect was associated with reduction of fasting blood glucose (r = −0.339, P = 0.023). This long-term study confirms that regular consumption of resveratrol can enhance cognitive and cerebrovascular functions in postmenopausal women, with the potential to slow cognitive decline due to ageing and menopause.

Hypoxia‐ischaemia (HI) can induce the death of cerebrovascular constituent cells through oxidative stress. Hydrogen is a powerful antioxidant which can activate the antioxidant system. A hypoxia‐ischaemia brain damage (HIBD) model was established in 7‐day‐old SD rats. Rats were treated with different doses of hydrogen‐rich water (HRW), and brain pericyte oxidative stress damage, cerebrovascular function and brain tissue damage were assessed. Meanwhile, in vitro‐cultured pericytes were subjected to oxygen–glucose deprivation and treated with different concentrations of HRW. Oxidative injury was measured and the molecular mechanism of how HRW alleviated oxidative injury of pericytes was also examined. The results showed that HRW significantly attenuated HI‐induced oxidative stress in the brain pericytes of neonatal rats, partly through the Nrf2‐HO‐1 pathway, further improving cerebrovascular function and reducing brain injury and dysfunction. Furthermore, HRW is superior to a single‐cell death inhibitor for apoptosis, ferroptosis, parthanatos, necroptosis and autophagy and can better inhibit HI‐induced pericyte death. The liver and kidney functions of rats were not affected by present used HRW dose. This study elucidates the role and mechanism of hydrogen in treating HIBD from the perspective of pericytes, providing new theoretical evidence and mechanistic references for the clinical application of hydrogen in neonatal HIE.

Background Accumulation of β-amyloid (Aβ) in the brain is a hallmark of Alzheimer’s Disease (AD). Cerebral deposition of Aβ initiates deteriorating pathways which eventually can lead to AD. However, the exact mechanisms are not known. A possible pathway could be that Aβ affects the cerebral vessels, causing inadequate cerebrovascular function. In the present study, we examined if Aβ accumulation is associated with a reduced cerebral blood flow response (CBF) to neuronal activation by visual stimulation (ΔCBF Vis.Act. ) in cognitively normal subjects from the Metropolit Danish Male Birth Cohort. Methods 64 subjects participated in the present study. ΔCBF Vis.Act. was measured using arterial spin labelling (ASL) combined with blood-oxygen-level-dependent (BOLD) MRI. Neuronal activation was obtained by visual stimulation by a flickering checkerboard presented on a screen in the MRI-scanner. Brain Aβ accumulation and cerebral glucose metabolism were assessed by PET imaging using the radiotracers [ 11 C]Pittsburgh Compound-B (PiB) and [ 18 F]Fluorodeoxyglucose (FDG), respectively. Cortical thickness was measured from structural MRI. Results ΔCBF Vis.Act. correlated negatively ( β = -32.1 [95% confidence interval (CI): -60.2; -4.1], r  = -0.30, p  = 0.025) with PiB standardized uptake value ratio (SUVr) in the brain regions activated by visual stimulation. ΔCBF Vis.Act. did not correlate with FDG SUVr ( β = 1.9 [CI: -23.8; 27.6], r  = 0.02, p  = 0.88) or cortical thickness ( β = 10.3 [CI: -8.4; 29.0], r  = 0.15, p  = 0.27) in the activated brain regions. Resting CBF did not correlate with PiB SUVr neither in the regions activated by visual stimulation ( β = -17.8 [CI:-71.9; 36.2], r  =- 0.09, p  = 0.51) nor in the remaining cortex ( β = 5.2 [CI:-3.9; 14.2], r  = 0.15, p  = 0.26). Conclusion We found a correlation between high PiB SUVr and reduced CBF response to neuronal activation, indicating a link between Aβ accumulation and impaired cerebrovascular function. The impairment was not associated with cortical thinning or hypometabolism, suggesting that Aβ accumulation affecting brain vessel function could be a very early pathology leading to neurodegenerative disease.

INTRODUCTION Cerebrovascular dysfunction may contribute to Alzheimer's disease (AD) pathogenesis. We examined how novel cerebral hemodynamic markers relate to neuroimaging phenotypes associated with AD dementia in cognitively impaired and unimpaired older adults. METHODS Statistical hemodynamic indices were computed for each participant from stochastic dynamic models relating resting‐state spontaneous arterial blood pressure and end‐tidal CO2 fluctuations to transcranial doppler‐derived blood velocity and near infrared spectroscopy‐derived cortical tissue oxygenation. Linear regressions related these hemodynamic indices to hippocampal volume, WMH volume, cortical thickness in an AD‐signature region, and brain amyloid burden measured by PET. RESULTS Higher hemodynamic indices, indicating proximity to normal cerebrovascular function correlated with neuroimaging phenotypes typically associated with better cognitive status: greater hippocampal volume and lower amyloid burden. DISCUSSION Our findings provide further support for the role of cerebrovascular dysfunction in AD pathogenesis and for the potential clinical utility of model‐based indices of cerebral hemodynamics. Highlights Model‐based hemodynamic marker estimation involves no effort from the participant. All hemodynamic indices differ between cognitively impaired and unimpaired adults. Novel hemodynamic markers correlate with established ADRD‐related brain phenotypes. Near‐infrared spectroscopy‐derived indices correlate with hippocampal volume. Dynamic cerebral autoregulation correlates with amyloid burden.

INTRODUCTION In a nested case–control study, we examined how cerebral perfusion relates to cognitive status and amyloid in the oldest‐old (i.e., 90 years of age and older). METHODS Study participants included 113 dementia‐free older adults (76 cognitively normal [CN]; 37 cognitively impaired, no dementia [CIND]) from the 90+ Study (mean age = 92.9, SD = 2.4). We quantified regional perfusion from arterial spin labeling‐MRI (magnetic resonance imaging) and amyloid deposition from florbetapir‐positron emission tomography (PET) in a region comprising the posterior cingulate and precuneus (PCC+PCu), and additionally quantified perfusion in other regions important for cognitive decline (medial temporal lobe, inferior parietal lobe, and orbitofrontal cortex). RESULTS Participants with CIND displayed lower perfusion in the PCC+PCu relative to participants who were CN, but there was no statistically significant difference between the groups in amyloid burden in this region. In addition, participants with CIND exhibited lower inferior parietal and higher orbitofrontal perfusion. DISCUSSION Cerebral perfusion is related to cognitive status in the oldest‐old independent of amyloidosis. Highlights Cerebral perfusion and amyloid positron emission tomography (PET) were measured in older adults: 90 years of age and older. Perfusion but not amyloid differed between cognitively impaired and normal groups. Frontal and parietal regions linked to cognitive decline had altered perfusion. Perfusion is related to cognitive status in the oldest‐old independent of amyloid.