Two surgical strategies (early carotid reperfusion vs. Central aortic repair-first) of acute type a aortic dissection complicated with cerebral malperfusion syndrome: a meta-analysis and systematic review.

OBJECTIVE: Cerebral malperfusion (CM) is a common comorbidity in acute type A aortic dissection (ATAAD), which is associated with high mortality and poor neurological prognosis. This meta-analysis investigated the surgical strategy of ATAAD patients with CM, aiming to compare the difference in therapeutic effectiveness between the central repair-first and the early reperfusion-first according to clinical outcomes. METHODS: The meta-analysis and systematic review was conducted based on studies sourced from the PubMed, Embase, and Cochrane literature database, in which cases of ATAAD with CM underwent surgical repair were included. Data for baseline characteristics, mortality, survival were extracted, and risk ratio (RR) values and the pooled mortality were calculated. RESULTS: A total of 17 retrospective studies were analyzed, including 1010 cases of ATAAD with CM underwent surgical repair. The pooled early mortality in early reperfusion group was lower (8.1%; CI, 0.02 to 0.168) than that in the central repair group (16.2%; CI, 0.115 to 0.216). The pooled long-term mortality was 7.9% in the early reperfusion cohort and 17.4% the central repair-first cohort, without a statistically significant heterogeneity (I [2] = 51.271%; p = 0.056). The mean time of symptom-onset-to-the-operation-room in all the reports was 8.87 ± 12.3 h. CONCLUSION: This meta-analysis suggested that early reperfusion-first may achieved better outcomes compared to central repair-first in ATAAD patients complicated with CM to some extent. Early operation and early restoration of cerebral perfusion may reduce the occurrence of some neurological complications. TRIAL REGISTRATION: The meta-analysis was registered in the International Prospective Register of Systematic Reviews database (No. CRD CRD42023475629) on Nov. 8th, 2023.

Imaging and blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease.

OBJECTIVE: To explore the imaging and transcranial Doppler cerebral blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease. METHODS: A retrospective analysis was conducted on the imaging data of 194 patients with cerebrovascular fenestration malformation who visited the Heyuan People's Hospital from July 2021 to July 2023. The location and morphology of the fenestration malformation blood vessels as well as the presence of other cerebrovascular diseases were analyzed. Transcranial Doppler cerebral blood flow detection data of patients with cerebral infarction and those with basilar artery fenestration malformation were also analyzed. RESULTS: A total of 194 patients with cerebral vascular fenestration malformation were found. Among the artery fenestration malformation, basilar artery fenestration was the most common, accounting for 46.08% (94/194). 61 patients (31.44%) had other vascular malformations, 97 patients (50%) had cerebral infarction, of which 30 were cerebral infarction in the fenestrated artery supply area. 28 patients with cerebral infarction in the fenestrated artery supply area received standardized antiplatelet, lipid-lowering and plaque-stabilizing medication treatment. During the follow-up period, these patients did not experience any symptoms of cerebral infarction or transient ischemic attack again. There were no differences in peak systolic flow velocity and end diastolic flow velocity, pulsatility index and resistance index between the ischemic stroke group and the no ischemic stroke group in patients with basal artery fenestration malformation (P > 0.05). CONCLUSION: Cerebrovascular fenestration malformation is most common in the basilar artery. Cerebrovascular fenestration malformation may also be associated with other cerebrovascular malformations. Standardized antiplatelet and statin lipid-lowering and plaque-stabilizing drugs are suitable for patients with cerebral infarction complicated with fenestration malformation. The relationship between cerebral blood flow changes in basilar artery fenestration malformation and the occurrence of ischemic stroke may not be significant.

[Impairment of attention and executive functions in chronic cerebrovascular disease and Alzheimer's disease]. / Narushenie vnimaniya i upravlyayushchikh funktsii pri sosudistykh kognitivnykh narusheniyakh i bolezni Al'tsgeimera.

OBJECTIVE: To establish specific features of executive functions (EF) impairment and attention in vascular cognitive impairment (VCI) and Alzheimer's disease (AD). MATERIAL AND METHODS: Eighty people (over the age of 50) diagnosed with cerebrovascular disease (CVD) and AD, as well as 29 healthy volunteers (control group), were examined. The following neuropsychological methods were used to study the quantitative and qualitative characteristics of cognitive impairments: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), EXIT-25, Frontal Assessment Battery (FAB), Clock Drawing Test, «12 Words¼ test, verbal associations (literal and categorical) method, Trail Making Test A and B, Symbol-Digit Modalities Test (SDMT), Stroop Test, and Benton Visual Retention Test. Mandatory inclusion criteria in the study included having a completed magnetic resonance imaging (MRI) of the brain (in T1, T2, FLAIR, DWI, SWI modes) within 1 year before enrollment in one of the groups. RESULTS: No significant differences in age, sex, and level of education were found between the groups. Groups AD and CVD were also comparable in the severity of cognitive impairment overall. Attention and working memory deficits were observed in both CVD and AD, with slightly more pronounced deficits in the AD group. Qualitative analysis of individual components of working memory revealed that both CVD and AD groups had comparable cognitive control impairment compared to the control group, while AD was characterized by a more significant decrease in intellectual flexibility compared to CVD. Sustained attention was equally impaired among patients in the CVD and AD groups, with a significant difference from the control group (p<0.05). In terms of memory, it was found that auditory-verbal memory and semantic memory were significantly more affected in AD, while visual memory was impaired in both conditions. CONCLUSION: Attention and EF impairments are not specific to the «subcortical¼ type of cognitive disorders. Already in the early stages, AD is characterized by a significant impairment of attention and EF, and such a component of EF as intellectual flexibility suffers at the onset of AD to a greater extent than in VCI. Memory impairments are not specific to AD; already at the onset of VCI, visual memory impairment comparable to AD is noted. The obtained data can be used for early neuropsychological diagnosis and differential diagnosis of dementing cerebral diseases.

Associations of cardiac function and arterial stiffness with cerebrovascular disease.

BACKGROUND: White matter hyperintensities (WMHs) represent diffuse small vessel disease implicating the cardiac, systemic, and cerebral vasculatures. As the brain may be the end-organ of cumulative vascular disease, and higher education is protective of both cardiovascular and brain health, we aim to clarify their intertwining relationships. METHODS: We evaluated participants (mean age = 64) from the UK Biobank with neuroimaging measures of WMHs, left ventricular ejection fraction (LVEF) quantified using cardiovascular MRI, and arterial stiffness index (ASI) quantified using finger photoplethysmography. We used multiple regression to evaluate the basic, independent, and interactive relationships of LVEF status (n = 27,512) and ASI (n = 33,584) with WMHs. Moderated mediation analysis was used to determine whether the relationship between LVEF status and WMH was mediated by ASI and moderated by education. RESULTS: Abnormal LVEF (ß = -0.082, p < 0.001) and higher ASI (ß = 0.02, p < 0.001) were associated with greater WMHs separately and independently, but not interactively. Moderated mediation analyses revealed that the relationship between abnormal LVEF and WMH was mediated by ASI, for individuals with lower education (ß = -0.004, p < 0.001). Abnormal LVEF was associated with lower cortical thickness in 16 predominantly frontotemporal and select parietal regions (FDR, q < 0.05). CONCLUSIONS: Cardiovascular dysfunction is associated with regional cerebral atrophy and may precipitate cerebrovascular disease via stiffening of systemic vasculatures, particularly for individuals with lower education. Integrative approaches to study biophysiological vascular systems can elucidate the complex interplay between biological and social determinants of brain and cerebrovascular health.

Accelerated decline in motor suppression in patients with cerebrovascular disorders: A kinetic analysis using the square-tracing task.

BACKGROUND: Patients with cerebrovascular disorders (CVDs) tend to exhibit impulsive behaviour without controlling their movements, leading to difficulty in performing activities of daily living and an increased risk of accidents. This hastiness, termed 'pacing impairment', has been studied but is not fully understood. OBJECTIVE: To experimentally examine the kinetic features of pacing impairment by focusing on changes in speed and investigating neuropsychological substrates. METHODS: We instructed 53 inpatients with CVDs, 20 orthopaedic inpatients, and 20 healthy participants to trace a 200 mm-sided square as slowly as possible for 120 seconds. We measured the tracing length and mean acceleration and examined the relationship between these measurements, neuropsychological symptoms, and lesion sites. RESULTS: Gradual acceleration in drawing, i.e., decline in motor suppression, was observed more frequently in the CVD group than in the control groups. Excessive acceleration was associated with unilateral spatial neglect, frontal lobe signs, and attention disorders but not with motor impersistence. Additionally, the incidence of excessive acceleration did not differ between left and right hemisphere lesion subgroups and was not associated with any specific lesion site. CONCLUSION: Pacing impairment can manifest as general or holistic deficits in attentional function widely distributed throughout the cerebral hemispheres.

Transcranial Doppler cerebrovascular reactivity: Thresholds for clinical significance in cerebrovascular disease.

BACKGROUND AND PURPOSE: Thresholds for abnormal transcranial Doppler cerebrovascular reactivity (CVR) studies are poorly understood, especially for patients with cerebrovascular disease. Using a real-world cohort with cerebral arterial stenosis, we sought to describe a clinically significant threshold for carbon dioxide reactivity (CO2R) and vasomotor range (VMR). METHODS: CVR studies were performed during conditions of breathing room air normally, breathing 8% carbon dioxide air mixture, and hyperventilation. The mean and standard deviation (SD) of CO2R and VMR were calculated for the unaffected side in patients with unilateral stenosis; a deviation of 2 SDs below the mean was chosen as the threshold for abnormal. Receiver operating characteristic (ROC) curves for both sides for patients with unilateral and bilateral stenosis were evaluated for sensitivity (Sn) and specificity (Sp). RESULTS: A total of 133 consecutive CVR studies were performed on 62 patients with stenosis with mean±SD age 55±16 years. Comorbidities included hypertension (60%), diabetes (15%), stroke (40%), and smoking (35%). In patients with unilateral stenosis, mean±SD CO2R for the unaffected side was 1.86±0.53%, defining abnormal CO2R as <0.80%. Mean±SD CO2R for the affected side was 1.27±0.90%. The CO2R threshold predicted abnormal acetazolamide single-photon emission computed tomography (SPECT) (Sn = .73, Sp = .79), CT/MRI perfusion abnormality (Sn = .42, Sp = .77), infarction on MRI (Sn = .45, Sp = .76), and pressure-dependent exam (Sn = .50, Sp = .76). For the unaffected side, mean±SD VMR was 39.5±15.8%, defining abnormal VMR as <7.9%. For the affected side, mean±SD VMR was 26.5±17.8%. The VMR threshold predicted abnormal acetazolamide SPECT (Sn = .46, Sp = .94), infarction on MRI (Sn = .27, Sp = .94), and pressure-dependent exam (Sn = .31, Sp = .90). CONCLUSIONS: In patients with multiple vascular risk factors, a reasonable threshold for clinically significant abnormal CO2R is <0.80% and VMR is <7.9%. Noninvasive CVR may aid in diagnosing and risk stratifying patients with stenosis.

Polysaccharide from Ganoderma lucidum alleviates cognitive impairment in a mouse model of chronic cerebral hypoperfusion by regulating CD4+CD25+Foxp3+ regulatory T cells.

Ganoderma lucidum (G. lucidum) is a kind of edible and medicinal mushroom. G. lucidum polysaccharide-1 (GLP-1) is one of the polysaccharides purified from crude GLP. Chronic cerebral hypoperfusion (CCH) as the common pathological basis of various forms of dementia is an important cause of cognitive impairment. In this study, a step-down test was used to evaluate the cognitive ability of CCH mice. Flow cytometry was used to detect the proportion of CD4+CD25+Foxp3+ regulatory T (Foxp3+Treg) cells. ELISA analysis and western blot analysis were used to detect the transforming growth factor-ß1 (TGF-ß1) and Interleukin-10 (IL-10) levels that Foxp3+Treg cells secreted. Metabolomic analysis based on gas chromatography-mass spectrometry (GC-MS) was used to evaluate the effect of GLP-1 on dysfunctional metabolism caused by inflammation. Results indicate that GLP-1 exhibited an alleviating cognitive impairment effect on CCH mice. The mechanism was related to GLP-1 by increasing Foxp3+Treg cell levels to increase levels of IL-10 and TGF-ß1 and regulate abnormal energy metabolism. These findings could provide preliminary results to exploit G. lucidum as a health care product or functional food for the adjuvant therapy of cognitive impairment of CCH.

Inflammation and the Link to Vascular Brain Health: Timing Is Brain.

Inflammation and its myriad pathways are now recognized to play both causal and consequential roles in vascular brain health. From acting as a trigger for vascular brain injury, as evidenced by the COVID-19 pandemic, to steadily increasing the risk for chronic cerebrovascular disease, distinct inflammatory cascades play differential roles in varying states of cerebrovascular injury. New evidence is regularly emerging that characterizes the role of specific inflammatory pathways in these varying states including those at risk for stroke and chronic cerebrovascular injury as well as during the acute, subacute, and repair phases of stroke. Here, we aim to highlight recent basic science and clinical evidence for many distinct inflammatory cascades active in these varying states of cerebrovascular injury. The role of cerebrovascular infections, spotlighted by the severe acute respiratory syndrome coronavirus 2 pandemic, and its association with increased stroke risk is also reviewed. Rather than converging on a shared mechanism, these emerging studies implicate varied and distinct inflammatory processes in vascular brain injury and repair. Recognition of the phasic nature of inflammatory cascades on varying states of cerebrovascular disease is likely essential to the development and implementation of an anti-inflammatory strategy in the prevention, treatment, and repair of vascular brain injury. Although advances in revascularization have taught us that time is brain, targeting inflammation for the treatment of cerebrovascular disease will undoubtedly show us that timing is brain.

Risk Factors, Lifestyle Behaviors, and Vascular Brain Health.

Although a relationship between traditional cardiovascular risk factors and stroke has long been recognized, these risk factors likely play a role in other aspects of brain health. Clinical stroke is only the tip of the iceberg of vascular brain injury that includes covert infarcts, white matter hyperintensities, and microbleeds. Furthermore, an individual's risk for not only stroke but poor brain health includes not only these traditional vascular risk factors but also lifestyle and genetic factors. The purpose of this narrative review is to summarize the state of the evidence on traditional and nontraditional vascular risk factors and their contributions to brain health. Additionally, we will review important modifiers that interact with these risk factors to increase, or, in some cases, reduce risk of adverse brain health outcomes, with an emphasis on genes and biomarkers associated with Alzheimer disease. Finally, we will consider the importance of social determinants of health in brain health outcomes.

Vascular Contributions to Brain Health: Cross-Cutting Themes.

As life expectancy grows, brain health is increasingly seen as central to what we mean by successful aging-and vascular brain health as central to overall brain health. Cerebrovascular pathologies are highly prevalent independent contributors to age-related cognitive impairment and at least partly modifiable with available treatments. The current Focused Update addresses vascular brain health from multiple angles, ranging from pathophysiologic mechanisms and neuroimaging features to epidemiologic risk factors, social determinants, and candidate treatments. Here we highlight some of the shared themes that cut across these distinct perspectives: (1) the lifetime course of vascular brain injury pathogenesis and progression; (2) the scientific and ethical imperative to extend vascular brain health research in non-White and non-affluent populations; (3) the need for improved tools to study the cerebral small vessels themselves; (4) the potential role for brain recovery mechanisms in determining vascular brain health and resilience; and (5) the cross-pathway mechanisms by which vascular and neurodegenerative processes may interact. The diverse perspectives featured in this Focused Update offer a sense of the multidisciplinary approaches and collaborations that will be required to launch our populations towards improved brain health and successful aging.

Acute cerebral venous outflow obstruction during convexity meningioma resection.

BACKGROUND: Cerebral venous outflow obstruction involves idiopathic intracranial hypertension, and the most common related condition is dural venous sinus stenosis or, in other words, an obstruction of the dural venous sinuses. In these cases, the pathological process is often chronic, displays only mild symptoms, and rarely requires urgent surgical intervention. In this study, we present a unique case involving an acute cerebral venous outflow obstruction that occurred during meningioma resection that ultimately had catastrophic consequences. MATERIALS AND METHODS: The patient's preoperative imaging only revealed an unremarkable frontal convexity meningioma with an average diameter exceeding 8 cm. She was admitted for a scheduled right frontoparietal craniotomy for lesion resection. RESULTS: The patient's unique congenital dural venous sinus structure along with a non-surgical epidural hematoma both contributed to a catastrophic outcome, causing a progressive hemispheric encephalocele, significant blood loss, and wound closure difficulties. CONCLUSION: Neurosurgeons should place an additional focus on cerebral venous outflow patency during tumor resection, even if the tumor does not involve the transverse or sigmoid sinuses. It is well known that the tacking sutures play an essential role in preventing an epidural hematoma, but the procedure to mitigate hematomas occurring outside the surgical field of view is not fully recognized by neurosurgeons. If dural tacking sutures are placed after complete tumor resection, the prophylactic effect for preventing EDH in the non-surgical areas may not be guaranteed. Therefore, we strongly advocate for the tacking sutures to be accurately placed before dural incisions are made.

Modifications in Near Infrared Spectroscopy for Cerebral Monitoring During Carotid Endarterectomy in Asymptomatic and Symptomatic Patients.

BACKGROUND: To evaluate trends and differences in Near Infrared Spectroscopy (NIRS) monitoring during carotid endarterectomy (CEA) in patients affected by asymptomatic and symptomatic carotid artery stenosis, to predict postoperative neurological complications (PNCs). METHODS: NIRS data of CEAs performed in a University Hospital were retrospectively reviewed. All the interventions were performed under general anesthesia and patients with intraoperative complications were excluded. Mean regional Oxygen Saturation Index (rSO2), pre-clamp values (mean baseline value, MBv and Single Mark Baseline value, SMBv) were collected and compared to the lowest rSO2 values during carotid cross-clamp (LSO2v) calculated within 3 min (percentage drop, PD). ROC curve analysis with Youden's Test was performed to determine the best threshold value of PD, in order to identify PNCs in both asymptomatic and symptomatic groups. RESULTS: Between 2007 and 2015, a total of 399 CEAs were consecutively performed with NIRS monitoring. Three-hundred-seventy-two CEAs in 355 patients were reviewed. Asymptomatic stenoses were 291 (81.9%), eleven (2.9%) PNC were registered (5 in asymptomatic and 6 in symptomatic group). Asymptomatic and symptomatic diseases had different MBv (69.5 ± 7.5 vs. 71.8 ± 6.9, respectively; P = 0.011) and similar rSO2 value during carotid clamping (63.7 ± 8.0 vs. 63.7 ± 6.7, respectively: P = 0.958). Asymptomatic patients experiencing PNCs had a greater PD than non-PNCs group (20.5 ± 10.2% vs. 12.5 ± 7.6%, respectively using MBv as baseline value; P = 0.002), in contrast, in symptomatic patients, in which a low PD was associated with PNCs, it does not reach statistical significance (using MBv, 12.6 ± 5.4% vs. 14.8 ± 6.7%, respectively; P= 0.476). In order to detect PNCs, ROC analysis revealed an optimal PD cut-off value of -17% in asymptomatic CEAs. (Sensibility (Se) 0.80, Specificity (Sp) 0.76, PPV 0.05, NPV 0.99, Youden's index 0.56; P = 0.020) In symptomatic a threshold value of -9% was found, without reaching statistical significance. CONCLUSIONS: NIRS as cerebral monitoring during CEA can predict PNCs in asymptomatic stenosis. Asymptomatic and symptomatic groups differ in baseline and intraprocedural cut-off values to detect an augmented PNCs risk.

Cerebrovascular alterations in NAFLD: Is it increasing our risk of Alzheimer's disease?

Non-alcoholic fatty liver disease (NAFLD) is a multisystem disease, which has been classified as an emerging epidemic not only confined to liver-related morbidity and mortality. It is also becoming apparent that NAFLD is associated with moderate cerebral dysfunction and cognitive decline. A possible link between NAFLD and Alzheimer's disease (AD) has only recently been proposed due to the multiple shared genes and pathological mechanisms contributing to the development of these conditions. Although AD is a progressive neurodegenerative disease, the exact pathophysiological mechanism remains ambiguous and similarly to NAFLD, currently available pharmacological therapies have mostly failed in clinical trials. In addition to the usual suspects (inflammation, oxidative stress, blood-brain barrier alterations and ageing) that could contribute to the NAFLD-induced development and progression of AD, changes in the vasculature, cerebral perfusion and waste clearance could be the missing link between these two diseases. Here, we review the most recent literature linking NAFLD and AD, focusing on cerebrovascular alterations and the brain's clearance system as risk factors involved in the development and progression of AD, with the aim of promoting further research using neuroimaging techniques and new mechanism-based therapeutic interventions.

Relationship of Four Blood Pressure Indexes to Subclinical Cerebrovascular Diseases Assessed by Brain MRI in General Japanese Men.

AIM: The relationship of blood pressure (BP) indexes (systolic blood pressure [SBP], diastolic blood pressure [DBP], pulse pressure [PP], mean arterial pressure [MAP]) to subclinical cerebrovascular diseases (SCVDs) remains unclear. This study aimed to elucidate the relationship of four BP indexes measured at two visits on SCVDs assessed by magnetic resonance imaging (MRI) in general Japanese men. METHODS: In general Japanese men aged 40-79 years (N=616), office BP indexes were measured at two visits (Visits 1 [2006-2008] and 2 [2010-2014]). MRI images obtained on the third visit (2012-2015) were examined for prevalent SCVDs: lacunar infarction, periventricular hyperintensity (PVH), deep subcortical white matter hyperintensity (DSWMH), microbleeds, and intracranial artery stenosis (ICAS). Using a multivariable logistic regression analysis, we computed and estimated the odds ratio of each prevalent SCVD for one standard deviation higher BP indexes. The same analyses were performed using home BP. RESULTS: All four office BP indexes at both visits associated with lacunar infarction. Visit 1 and 2 DBP and Visit 1 MAP associated with PVH and DSWMH, and Visit 1 SBP associated with DSWMH. All Visit 2 BP indexes appear to show stronger association with microbleeds than Visit 1 indexes, and Visit 1 and 2 SBP, PP, and MAP showed similar associations with ICAS. Additional analyses using home BP indexes revealed similar relationships; however, the significance of some relationships decreased. CONCLUSION: In general Japanese men, BP indexes were associated with most of SCVDs, and BP indexes measured at different periods associated with different SCVDs assessed by MRI.

The impact of chronic mild hypoxia on cerebrovascular remodelling; uncoupling of angiogenesis and vascular breakdown.

BACKGROUND: Chronic mild hypoxia (CMH, 8% O2) stimulates robust vascular remodelling in the brain, but it also triggers transient vascular disruption. This raises the fundamental question: is the vascular leak an unwanted side-effect of angiogenic remodelling or is it a pathological response, unrelated to endothelial proliferation, in which declining oxygen levels trigger endothelial dysfunction? METHODS: To answer this question, mice were exposed to CMH (8% O2) for periods up to 14 days, after which, brain tissue was examined by immunofluorescence (IF) to determine which type of blood vessel (arteriole, capillary or venule) was most commonly associated with endothelial proliferation and vascular leak and how this correlated with tight junction protein expression. Vascular perfusion was examined using DiI. Data were analysed using one-way analysis of variance (ANOVA) followed by Tukey's multiple comparison post-hoc test. RESULTS: The following was observed: (1) most endothelial proliferation and extravascular fibrinogen leak occurred in capillaries and to a lesser degree in venules, (2) much to our surprise, endothelial proliferation and extravascular fibrinogen leak never colocalized, (3) interestingly however, endothelial proliferation was strongly associated with an intravascular fibrinogen staining pattern not seen in stable blood vessels, (4) DiI perfusion studies revealed that angiogenic vessels were adequately perfused, suggesting that fibrinogen retention in angiogenic vessels is not due to temporary closure of the vessel, but more likely because fibrinogen is retained within the vessel wall, (5) bromodeoxyuridine (BrdU) labelling as a means to more permanently label proliferating endothelial cells, confirmed lack of any connection between endothelial proliferation and extravascular fibrinogen leak, while (6) in contrast, proliferating microglia were detected within extravascular leaks. CONCLUSIONS: Taken together, our findings support the concept that in the short-term, hypoxia-induced endothelial proliferation triggers transient fibrinogen deposition within the walls of angiogenic blood vessels, but no overt vascular leak occurs in these vessels. Importantly, endothelial proliferation and extravascular fibrinogen leaks never co-localize, demonstrating that extravascular leak is not an unwanted side-effect of angiogenic endothelial proliferation, but rather a dysfunctional vascular response to hypoxia that occurs in a distinct group of non-angiogenic blood vessels.

Research on Association between Levels of Serum Adiponectin, Hs-CRP, and sICAM-1 and Hypertensive Cerebrovascular Complications.

The study is aimed at studying the association between the levels of serum adiponectin (ADPN), high-sensitivity C-reactive protein (hs-CRP), and soluble intercellular adhesion molecule-1 (sICAM-1) and hypertensive cerebrovascular complications. 50 patients with hypertensive cerebrovascular disease treated in Gansu Provincial Hospital from December 2016 to December 2018 were selected as the experimental group, and 50 normal people who underwent physical examination were selected as the control group. The blood pressure, heart rate, and the complications were recorded, and the serum blood lipid indexes were detected. Moreover, the content of serum ADPN, hs-CRP, and sICAM-1; the neurological indexes; brain-derived neurotrophic factor (BNDF); and neurone-specific enolase (NSE) were also determined using ELISA. The content of aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and serum creatinine (SCR) in the experimental group was significantly higher than that in control group (p < 0.05); the incidence of cerebrovascular complications, systolic blood pressure, diastolic blood pressure, and heart rate increased (p < 0.05); the content of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), hs-CRP, and sICAM-1 obviously rose (p < 0.05); and the content of ADPN and HDL obviously declined (p < 0.05). Besides, the experimental group had evidently lower systolic blood flow velocity (Vs), diastolic blood flow velocity (Vd), and mean blood flow velocity (Vm) and evidently higher pulsatility index (PI) (p < 0.05). The levels of S100 and NSE in the experimental group increased significantly, and the level of BNDF decreased significantly (p < 0.05). In patients with hypertensive cerebrovascular disease, the level of ADPN declines; the levels of hs-CRP and sICAM-1 rise; the incidence rate of cerebrovascular complications is elevated; and there are changes in the blood lipid, cerebrovascular hemodynamic, and neurological indexes, thereby further promoting the occurrence and development of hypertensive cerebrovascular disease.

Involvement of cerebrovascular abnormalities in the pathogenesis and progression of Alzheimer's disease: an adrenergic approach.

Alzheimer's disease (AD), as the most common neurodegenerative disease in elder population, is pathologically characterized by ß-amyloid (Aß) plaques, neurofibrillary tangles composed of highly-phosphorylated tau protein and consequently progressive neurodegeneration. However, both Aß and tau fails to cover the whole pathological process of AD, and most of the Aß- or tau-based therapeutic strategies are all failed. Increasing lines of evidence from both clinical and preclinical studies have indicated that age-related cerebrovascular dysfunctions, including the changes in cerebrovascular microstructure, blood-brain barrier integrity, cerebrovascular reactivity and cerebral blood flow, accompany or even precede the development of AD-like pathologies. These findings may raise the possibility that cerebrovascular changes are likely pathogenic contributors to the onset and progression of AD. In this review, we provide an appraisal of the cerebrovascular alterations in AD and the relationship to cognitive impairment and AD pathologies. Moreover, the adrenergic mechanisms leading to cerebrovascular and AD pathologies were further discussed. The contributions of early cerebrovascular factors, especially through adrenergic mechanisms, should be considered and treasured in the diagnostic, preventative, and therapeutic approaches to address AD.