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Aging is frequently associated with compromised cerebrovasculature and pericytes. However, we do not know how normal aging differentially impacts vascular structure and function in different brain areas. Here we utilize mesoscale microscopy methods and in vivo imaging to determine detailed changes in aged murine cerebrovascular networks. Whole-brain vascular tracing shows an overall ~10% decrease in vascular length and branching density with ~7% increase in vascular radii in aged brains. Light sheet imaging with 3D immunolabeling reveals increased arteriole tortuosity of aged brains. Notably, vasculature and pericyte densities show selective and significant reductions in the deep cortical layers, hippocampal network, and basal forebrain areas. We find increased blood extravasation, implying compromised blood-brain barrier function in aged brains. Moreover, in vivo imaging in awake mice demonstrates reduced baseline and on-demand blood oxygenation despite relatively intact neurovascular coupling. Collectively, we uncover regional vulnerabilities of cerebrovascular network and physiological changes that can mediate cognitive decline in normal aging. We have limited knowledge of how aging affects brain vascular structure and function. Here, the authors show that aging induces selective reduction of vasculature and related cell types in key cognitive brain areas and reduces blood oxygenation.

Nanothermometers enable the detection of temperature changes at the microscopic scale, which is crucial for elucidating biological mechanisms and guiding treatment strategies. However, temperature monitoring of micron-scale structures in vivo using luminescent nanothermometers remains challenging, primarily due to the severe scattering effect of biological tissue that compromises the imaging resolution. Herein, a lanthanide luminescence nanothermometer with a working wavelength beyond 1500 nm is developed to achieve high-resolution temperature imaging in vivo. The energy transfer between lanthanide ions (Er 3+ and Yb 3+ ) and H 2 O molecules, called the environment quenching assisted downshifting process, is utilized to establish temperature-sensitive emissions at 1550 and 980 nm. Using an optimized thin active shell doped with Yb 3+ ions, the nanothermometer’s thermal sensitivity and the 1550 nm emission intensity are enhanced by modulating the environment quenching assisted downshifting process. Consequently, minimally invasive temperature imaging of the cerebrovascular system in mice with an imaging resolution of nearly 200 μm is achieved using the nanothermometer. This work points to a method for high-resolution temperature imaging of micron-level structures in vivo, potentially giving insights into research in temperature sensing, disease diagnosis, and treatment development. The strong scattering of biological tissue causes challenges when monitoring temperature changes at the microscale. Here, the authors propose a nanothermometer based on lanthanide luminescence, enabling minimally invasive imaging of the cerebrovascular system of mice at nearly 200 μm resolution.

Brain fluids are rigidly regulated to provide stable environments for neuronal function, e.g., low K + , Ca 2+ , and protein to optimise signalling and minimise neurotoxicity. At the same time, neuronal and astroglial waste must be promptly removed. The interstitial fluid (ISF) of the brain tissue and the cerebrospinal fluid (CSF) bathing the CNS are integral to this homeostasis and the idea of a glia-lymph or ‘glymphatic’ system for waste clearance from brain has developed over the last 5 years. This links bulk (convective) flow of CSF into brain along the outside of penetrating arteries, glia-mediated convective transport of fluid and solutes through the brain extracellular space (ECS) involving the aquaporin-4 (AQP4) water channel, and finally delivery of fluid to venules for clearance along peri-venous spaces. However, recent evidence favours important amendments to the ‘glymphatic’ hypothesis, particularly concerning the role of glia and transfer of solutes within the ECS. This review discusses studies which question the role of AQP4 in ISF flow and the lack of evidence for its ability to transport solutes; summarizes attributes of brain ECS that strongly favour the diffusion of small and large molecules without ISF flow; discusses work on hydraulic conductivity and the nature of the extracellular matrix which may impede fluid movement; and reconsiders the roles of the perivascular space (PVS) in CSF–ISF exchange and drainage. We also consider the extent to which CSF–ISF exchange is possible and desirable, the impact of neuropathology on fluid drainage, and why using CSF as a proxy measure of brain components or drug delivery is problematic. We propose that new work and key historical studies both support the concept of a perivascular fluid system, whereby CSF enters the brain via PVS convective flow or dispersion along larger caliber arteries/arterioles, diffusion predominantly regulates CSF/ISF exchange at the level of the neurovascular unit associated with CNS microvessels, and, finally, a mixture of CSF/ISF/waste products is normally cleared along the PVS of venules/veins as well as other pathways; such a system may or may not constitute a true ‘circulation’, but, at the least, suggests a comprehensive re-evaluation of the previously proposed ‘glymphatic’ concepts in favour of a new system better taking into account basic cerebrovascular physiology and fluid transport considerations.

Intravascular imaging has emerged as a valuable tool for the treatment of coronary and peripheral artery disease; however, no solution is available for safe and reliable use in the tortuous vascular anatomy of the brain. Endovascular treatment of stroke is delivered under image guidance with insufficient resolution to adequately assess underlying arterial pathology and therapeutic devices. High-resolution imaging, enabling surgeons to visualize cerebral arteries' microstructure and micron-level features of neurovascular devices, would have a profound impact in the research, diagnosis, and treatment of cerebrovascular diseases. Here, we present a neurovascular high-frequency optical coherence tomography (HF-OCT) system, including an imaging console and an endoscopic probe designed to rapidly acquire volumetric microscopy data at a resolution approaching 10 microns in tortuous cerebrovascular anatomies. Using a combination of in vitro, ex vivo, and in vivo models, the feasibility of HF-OCT for cerebrovascular imaging was demonstrated. High resolution intravascular imaging in the brain is limited by the high tortuosity of the vasculature. Here the authors present a fiber optic imaging technology using high-frequency optical coherence tomography (HF-OCT) to provide volumetric high resolution images in the highly tortuous cerebral vasculature.

Purpose Takayasu arteritis (TA) is a rare, chronic, inflammatory large-vessel vasculitis that affects the aorta and its main branches, including the cerebrovascular system. This review analyzes current knowledge and patient outcomes concerning the cerebrovascular implications of TA. Methods A literature search, with publications from 1994 to 2024, identified pertinent studies through PubMed. An illustrative case report details a 19-year-old female with Type 1 TA, illustrating the complex decision required in the absence of surgical or endovascular options. Results Our results offer a demographic analysis of 1,698 TA patients, highlighting a female predominance of 89.99% and a mean symptom onset at 33 years. The clinical spectrum of cerebrovascular involvement presented varied symptoms, most notably dizziness, with significant incidences of ischemic events and bilateral stenosis primarily affecting the carotid and subclavian arteries. The most common type of TA was Type V, affecting 40% of patients studied. Endovascular treatment had a 95% initial success rate, with a 67% restenosis rate. Surgical treatment was successful in 84% of cases, but 21% had notable post-operative complications. Similar to the endovascular population, those treated with stand-alone conservative therapy saw a 93% initial remission rate with 52% having relapsed. Conclusion Assessing the disease activity of TA is crucial when planning vascular intervention due to its significant impact on treatment outcomes. Despite its greater initial invasiveness, surgical interventions showed lower restenosis rates compared to either endovascular interventions or standalone conservative management. We emphasize advancements in TA management and the pressing need for continued research into diagnostic and treatment protocols for improved patient outcomes.

Functional neuroimaging, such as fMRI, is based on coupling neuronal activity and accompanying changes in cerebral blood flow (CBF) and metabolism. However, the relationship between CBF and events at the level of the penetrating arterioles and capillaries is not well established. Recent findings suggest an active role of capillaries in CBF control, and pericytes on capillaries may be major regulators of CBF and initiators of functional imaging signals. Here, using two-photon microscopy of brains in living mice, we demonstrate that stimulation-evoked increases in synaptic activity in the mouse somatosensory cortex evokes capillary dilation starting mostly at the first- or second-order capillary, propagating upstream and downstream at 5–20 μm/s. Therefore, our data support an active role of pericytes in cerebrovascular control. The gliotransmitter ATP applied to first- and second-order capillaries by micropipette puffing induced dilation, followed by constriction, which also propagated at 5–20 μm/s. ATP-induced capillary constriction was blocked by purinergic P2 receptors. Thus, conducted vascular responses in capillaries may be a previously unidentified modulator of cerebrovascular function and functional neuroimaging signals.

Both intracranial pressure (ICP) and the cerebrovascular pressure reactivity represent the dysregulation of pathways directly involved in traumatic brain injury (TBI) pathogenesis and have been used to inform clinical management. However, how these parameters evolve over time following injury and whether this evolution has any prognostic importance have not been studied. We analysed the temporal profile of ICP and pressure reactivity index (PRx), examined their relation to TBI-specific mortality, and determined if the prognostic relevance of these parameters was affected by their temporal profile using mixed models for repeated measures of ICP and PRx for the first 240 hours from the time of injury. A total of 601 adults with TBI, admitted between September 2002 to January 2016, and with high-resolution continuous monitoring from a single centre, were studied. At 6 months postinjury, 133 (19%) patients had a fatal outcome; of those, 88 (78%) died from nonsurvivable TBI or brain death. The difference in mean ICP between those with a fatal outcome and functional survivors was only significant for the first 168 hours after injury (all p < 0.05). For PRx, those patients with a fatal outcome also had a higher (more impaired) PRx throughout the first 120 hours after injury (all p < 0.05). The separation of ICP and PRx was greatest in the first 72 hours after injury. Mixed models demonstrated that the explanatory power of the PRx decreases over time; therefore, the prognostic weight assigned to PRx should similarly decrease. However, the ability of ICP to predict a fatal outcome remained relatively stable over time. As control of ICP is the central purpose of TBI management, it is likely that some of the information that is reflected in the natural history of ICP changes is no longer apparent because of therapeutic intervention. We demonstrated the temporal evolution of ICP and PRx and their relationship with fatal outcome, indicating a potential early prognostic and therapeutic window. The combination of dynamic monitoring variables and their time profile improved prediction of outcome. Therefore, time-driven dynamic modelling of outcome in patients with severe TBI may allow for more accurate and clinically useful prediction models. Further research is needed to confirm and expand on these findings.

Transcatheter aortic-valve replacement with a new self-expanding prosthesis was compared with surgical aortic-valve replacement in patients with aortic stenosis who were at high surgical risk. The rate of death from any cause at 1 year was lower in the TAVR group. Aortic stenosis is a debilitating disease in elderly persons that carries a dismal prognosis after symptom onset. 1 Although surgical aortic-valve replacement remains the standard treatment for aortic stenosis, 2 many patients are not suitable candidates for surgical replacement owing to an increased risk of death during surgery. 3 , 4 Transcatheter aortic-valve replacement (TAVR) with a balloon-expandable device improves survival, as compared with medical therapy, in patients with severe aortic stenosis who cannot undergo surgery. 5 Balloon-expandable TAVR and surgical aortic-valve replacement are associated with similar survival rates at 1 year among patients considered to be at high surgical risk, although the frequency of . . .

Markers of the systemic inflammatory response, including C-reactive protein and albumin (combined to form the modified Glasgow Prognostic Score), as well as neutrophil, lymphocyte and platelet counts have been shown to be prognostic of survival in patients with cancer. The aim of the present study was to examine the prognostic relationship between these markers of the systemic inflammatory response and all-cause, cancer, cardiovascular and cerebrovascular mortality in a large incidentally sampled cohort. Patients (n = 160 481) who had an incidental blood sample taken between 2000 and 2008 were studied for the prognostic value of C-reactive protein (>10mg/l, albumin (>35mg/l), neutrophil (>7.5×109/l) lymphocyte and platelet counts. Also, patients (n = 52 091) sampled following the introduction of high sensitivity C-reactive protein (>3mg/l) measurements were studied. A combination of these markers, to make cumulative inflammation-based scores, were investigated. In all patients (n = 160 481) C-reactive protein (>10mg/l) (HR 2.71, p<0.001), albumin (>35mg/l) (HR 3.68, p<0.001) and neutrophil counts (HR 2.18, p<0.001) were independently predictive of all-cause mortality. These associations were also observed in cancer, cardiovascular and cerebrovascular mortality before and after the introduction of high sensitivity C-reactive protein measurements (>3mg/l) (n = 52 091). A combination of high sensitivity C-reactive protein (>3mg/l), albumin and neutrophil count predicted all-cause (HR 7.37, p<0.001, AUC 0.723), cancer (HR 9.32, p<0.001, AUC 0.731), cardiovascular (HR 4.03, p<0.001, AUC 0.650) and cerebrovascular (HR 3.10, p<0.001, AUC 0.623) mortality. The results of the present study showed that an inflammation-based prognostic score, combining high sensitivity C-reactive protein, albumin and neutrophil count is prognostic of all-cause mortality.

To investigate whether changes in cerebrovascular hemodynamic parameters during extracorporeal membrane oxygenation (ECMO) treatment in neonates are associated with the occurrence of cerebrovascular complications. This study selected neonatal patients who received ECMO treatment at a pediatric hospital in China from June 2021 to June 2024. Relevant clinical data were collected from the electronic medical record system. Data from cranial ultrasound examinations before and during ECMO treatment, as well as the occurrence of cerebrovascular complications, were collected for further analysis. A total of 37 neonates were enrolled in this study. Among them, 15 neonates who developed cerebrovascular complications during ECMO were included in the complication group, while the remaining 22 neonates were included in the non-complication group. The age difference between the two groups was statistically significant. The systolic blood pressure coefficient of variation (SBP-CV) and diastolic blood pressure CV (DBP-CV) were significantly higher in the complication group compared to the non-complication group. Additionally, the anterior cerebral artery peak systolic velocity CV (ACA-PSV-CV) and ACA resistance index CV (ACA-RI-CV) were significantly higher in the complication group than in the non-complication group. However, there was no significant difference in the ACA end-diastolic velocity CV (ACA-EDV-CV) between the two groups. The receiver operating characteristic (ROC) curve analysis of risk factors for cerebrovascular complications indicated that the area under the curve (AUC) for ACA-RI-CV was 0.765 (95% CI: 0.608-0.923, p = 0.007). The AUC for ACA-SBP-CV was 0.815 (95% CI: 0.666-0.964, p = 0.001). Moreover, when ACA-RI-CV and ACA-SBP-CV were combined, the AUC was 0.873 (95% CI: 0.758-0.988, p<0.001). High ACA-RI-CV and ACA-SBP-CV were associated with the occurrence of cerebrovascular complications during ECMO treatment in neonates. The combined detection of ACA-RI-CV and ACA-SBP-CV had a predictive role in the early identification of cerebrovascular complications in neonatal ECMO patients.