Artificial dural regeneration matrix as a substitute for autologous tissue in indirect bypass in Moyamoya disease: Investigation of a rat model of chronic cerebral hypoperfusion.

Indirect bypass using autologous tissue is effective in Moyamoya disease, especially among pediatric patients. This study aimed to evaluate the effectiveness of indirect bypass using DuraGen (absorbable artificial dura mater composed of collagen matrix), as a substitute for autologous tissue in a rat model of chronic cerebral hypoperfusion. Male Wistar rats were subjected to bilateral internal carotid artery occlusion and divided into three groups: a control group without bypass surgery, a group wherein indirect bypass was performed using the temporalis muscle (encephalo-myo-synangiosis [EMS] group), and a group wherein DuraGen was used (Dura group).

tPA supplementation preserves neurovascular and cognitive function in Tg2576 mice.

Introduction: Amyloid beta (Aβ) impairs the cerebral blood flow (CBF) increase induced by neural activity (functional hyperemia). Tissue plasminogen activator (tPA) is required for functional hyperemia, and in mouse models of Aβ accumulation tPA deficiency contributes to neurovascular and cognitive impairment. However, it remains unknown if tPA supplementation can rescue Aβ-induced neurovascular and cognitive dysfunction.

Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress.

Background: Cerebral amyloid angiopathy (CAA) is a devastating condition common in patients with Alzheimer's disease but also observed in the general population. Vascular oxidative stress and neurovascular dysfunction have been implicated in CAA but the cellular source of reactive oxygen species (ROS) and related signaling mechanisms remain unclear. We tested the hypothesis that brain border-associated macrophages (BAM), yolk sac-derived myeloid cells closely apposed to parenchymal and leptomeningeal blood vessels, are the source of radicals through the Aβ-binding innate immunity receptor CD36, leading to neurovascular dysfunction, CAA, and cognitive impairment.

Pretreatment with Clodronate Improved Neurological Function by Preventing Reduction of Posthemorrhagic Cerebral Blood Flow in Experimental Subarachnoid Hemorrhage.

Background: Brain perivascular macrophages (PVMs) are potential treatment targets for subarachnoid hemorrhage (SAH), and previous studies revealed that their depletion by clodronate (CLD) improved outcomes after experimental SAH. However, the underlying mechanisms are not well understood. Therefore, we investigated whether reducing PVMs by CLD pretreatment improves SAH prognosis by inhibiting posthemorrhagic impairment of cerebral blood flow (CBF).

Two children with lymphocytic hypophysitis presenting with positive anti-rabphilin-3A antibody.

Lymphocytic hypophysitis (LYH) is a rare chronic inflammatory disease characterized by lymphocytic infiltration of the anterior or posterior pituitary gland and hypothalamus. LYH is subdivided into lymphocytic adenohypophysitis (LAH), lymphocytic infundibulo-neurohypophysitis (LINH), and lymphocytic panhypophysitis (LPH) depending on the primary site. Most cases occur in adults, with few cases reported in children, and it is especially important to distinguish LYH from suprasellar malignancies, such as germ cell tumors and other neoplastic diseases.

Macrophage colony-stimulating factor potentially induces recruitment and maturation of macrophages in recurrent pituitary neuroendocrine tumors.

Although pituitary neuroendocrine tumors (PitNETs) are usually benign, some are highly invasive and recurrent. Recurrent PitNETs are often treatment-resistant and there is currently no effective evidence-based treatment. Tumor-associated macrophages (TAMs) promote tumor growth in many cancers, but the effect of TAMs on PitNETs remains unclear.

Bias for Treatment Effect by Measurement Error in Pretest in ANCOVA Analysis.

This paper investigated consequences of measurement error in the pretest on the estimate of the treatment effect in a pretest-posttest design with the analysis of covariance (ANCOVA) model, focusing on both the direction and magnitude of its bias. Some prior studies have examined the magnitude of the bias due to measurement error and suggested ways to correct it. However, none of them clarified how the direction of bias is affected by measurement error.

Intracranial and extracranial multiple arterial dissecting aneurysms in rheumatoid arthritis: A case report.

Objective: We describe a case of intracranial and extracranial multiple arterial dissecting aneurysms in rheumatoid arthritis (RA).

Case Presentation: A 29-year-old man with a medical history of RA since 18 years of age was admitted to our hospital for vomiting, dysarthria, and conscious disturbance. At 23, he underwent ligation of the left internal carotid artery (ICA) with superficial temporal artery to middle cerebral artery anastomosis because of acute infarct of the left hemisphere caused by arterial dissection of the left ICA.

Tau induces PSD95-neuronal NOS uncoupling and neurovascular dysfunction independent of neurodegeneration.

Cerebrovascular abnormalities have emerged as a preclinical manifestation of Alzheimer's disease and frontotemporal dementia, diseases characterized by the accumulation of hyperphosphorylated forms of the microtubule-associated protein tau. However, it is unclear whether tau contributes to these neurovascular alterations independent of neurodegeneration. We report that mice expressing mutated tau exhibit a selective suppression of neural activity-induced cerebral blood flow increases that precedes tau pathology and cognitive impairment.

Hemodynamic study about cortical hyperintensity belt sign after direct bypass surgery for moyamoya disease.

Transient neurological events (TNEs) are observed after direct bypass surgery in patients with moyamoya disease (MMD). Although a correlation between cortical hyperintensity belt signs (CHBs) and TNEs has been reported, the pathophysiology of CHBs is still unknown. The purpose of this study was to reveal the pathophysiology of CHBs by using dynamic susceptibility contrast-magnetic resonance imaging.

AGO CLIP Reveals an Activated Network for Acute Regulation of Brain Glutamate Homeostasis in Ischemic Stroke.

Post-transcriptional regulation by microRNAs (miRNAs) is essential for complex molecular responses to physiological insult and disease. Although many disease-associated miRNAs are known, their global targets and culminating network effects on pathophysiology remain poorly understood. We applied Argonaute (AGO) crosslinking immunoprecipitation (CLIP) to systematically elucidate altered miRNA-target interactions in brain following ischemia and reperfusion (I/R) injury.

Cortical Venous Reddening Predicts Remote Cerebral Infarction Post Superficial Temporal Artery-Middle Cerebral Artery Bypass in Atherosclerotic Occlusive Cerebrovascular Disease.

Background: The superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis (STA-MCA bypass) currently is performed to prevent atherosclerotic occlusive cerebrovascular disease. However, the benefits of the bypass surgery remain controversial. To ensure consistent surgical benefits, understanding the mechanisms of perioperative cerebral infarction (CI) is required.

Apoε4 disrupts neurovascular regulation and undermines white matter integrity and cognitive function.

The ApoE4 allele is associated with increased risk of small vessel disease, which is a cause of vascular cognitive impairment. Here, we report that mice with targeted replacement (TR) of the ApoE gene with human ApoE4 have reduced neocortical cerebral blood flow compared to ApoE3-TR mice, an effect due to reduced vascular density rather than slowing of microvascular red blood cell flow. Furthermore, homeostatic mechanisms matching local delivery of blood flow to brain activity are impaired in ApoE4-TR mice.

Role of ASK1/p38 Cascade in a Mouse Model of Alzheimer's Disease and Brain Aging.

To examine the role of ASK1 in Alzheimer's disease (AD), we generated 5XFAD mice deficient in ASK1 and investigated the characteristics of old 5XFAD and wild-type mice with ASK1 deficiency. ASK1 deficiency improved cognitive function in 24-month-old 5XFAD mice, which was associated with the reduction of phosphorylated p38. Thus, ASK1/p38 cascade seems to play some role in the pathogenesis of AD in mice.

Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides.

Rationale: Increasing evidence indicates that alterations of the cerebral microcirculation may play a role in Alzheimer disease, the leading cause of late-life dementia. The amyloid-β peptide (Aβ), a key pathogenic factor in Alzheimer disease, induces profound alterations in neurovascular regulation through the innate immunity receptor CD36 (cluster of differentiation 36), which, in turn, activates a Nox2-containing NADPH oxidase, leading to cerebrovascular oxidative stress. Brain perivascular macrophages (PVM) located in the perivascular space, a major site of brain Aβ collection and clearance, are juxtaposed to the wall of intracerebral resistance vessels and are a powerful source of reactive oxygen species.

Use of Paine's Technique: Projecting Puncture Point to the Skull and Skin.

Objective: Ventriculostomy from Paine's point is an effective technique to ensure that the brain is relaxed for aneurysm surgery. This study aimed to use Paine's point for other neurosurgical procedures (except for those that require a pterional approach) by delineation of surface landmarks for identification of Paine's point on the cranium and scalp.

Methods: Based on the anatomical knowledge and examination of 3-dimensional computed tomography images of skull, we determined novel surface landmarks to identify Paine's point on the cranium and scalp.

Chronic kidney disease accelerates cognitive impairment in a mouse model of Alzheimer's disease, through angiotensin II.

Epidemiological studies suggest that chronic kidney disease (CKD) is a significant risk factor in the development of cognitive decline. However, the exact role of CKD in cognitive impairment or dementia is unclear. This work was performed to examine the potential impact of CKD on cognitive impairment in Alzheimer's disease (AD), focusing on angiotensin II.

Obligatory Role of EP1 Receptors in the Increase in Cerebral Blood Flow Produced by Hypercapnia in the Mice.

Hypercapnia induces potent vasodilation in the cerebral circulation. Although it has long been known that prostanoids participate in the cerebrovascular effects of hypercapnia, the role of prostaglandin E2 (PGE2) and PGE2 receptors have not been fully investigated. In this study, we sought to determine whether cyclooxygenase-1 (COX-1)-derived PGE2 and EP1 receptors are involved in the cerebrovascular response induced by hypercapnia.