Journal articles: 'Brain parenchyma'

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Bueche, Celine Z., Cheryl Hawkes, Cornelia Garz, Stefan Vielhaber, Johannes Attems, Robert T. Knight, Klaus Reymann, Hans‐Jochen Heinze, Roxana O. Carare, and Stefanie Schreiber. "Hypertension drives parenchymal β‐amyloid accumulation in the brain parenchyma." Annals of Clinical and Translational Neurology 1, no. 2 (January 9, 2014): 124–29. http://dx.doi.org/10.1002/acn3.27.

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Hobohm, R. E., P. Codd, and M. D. Malinzak. "Ectopic Cerebellar Brain Parenchyma." Neurographics 9, no. 4 (August 1, 2019): 285–87. http://dx.doi.org/10.3174/ng.1800047.

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McCall, Anthony L., Antonia M. Van Bueren, Valerie Nipper, Melissa Moholt-Siebert, Hall Downes, and Nikola Lessov. "Forebrain Ischemia Increases Glut1 Protein in Brain Microvessels and Parenchyma." Journal of Cerebral Blood Flow & Metabolism 16, no. 1 (January 1996): 69–76. http://dx.doi.org/10.1097/00004647-199601000-00008.

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Glucose transport into nonneuronal brain cells uses differently glycosylated forms of the glucose transport protein, GLUT1. Microvascular GLUT1 is readily seen on immunocytochemistry, although its parenchymal localization has been difficult. Following ischemia, GLUT1 mRNA increases, but whether GLUT1 protein also changes is uncertain. Therefore, we examined the immunocytochemical distribution of GLUT1 in normal rat brain and after transient global forebrain ischemia. A novel immunocytochemical finding was peptide-inhibitable GLUT1 immunoreactive staining in parenchyma as well as in cerebral microvessels. In nonischemic rats, parenchymal GLUT1 staining co-localizes with glial fibrillary acidic protein (GFAP) in perivascular foot processes of astrocytes. By 24 h after ischemia, both microvascular and nonmicrovascular GLUT1 immunoreactivity increased widely, persisting at 4 days postischemia. Vascularity within sections of brain similarly increased after ischemia. Increased parenchymal GLUT1 expression was paralleled by staining for GFAP, suggesting that nonvascular GLUT1 overexpression may occur in reactive astrocytes. A final observation was a rapid expression of inducible heat shock protein (HSP)70 in hippocampus and cortex by 24 h after ischemia. We conclude that GLUT1 is normally immunocytochemically detectable in cerebral microvessels and parenchyma and that parenchymal expression occurs in some astroglia. After global cerebral ischemia, GLUT1 overexpression occurs rapidly and widely in microvessels and parenchyma; its overexpression may be related to an immediate early-gene form of response to cellular stress.

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Yokel, Robert A. "Nanoparticle brain delivery: a guide to verification methods." Nanomedicine 15, no. 4 (February 2020): 409–32. http://dx.doi.org/10.2217/nnm-2019-0169.

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Many reports conclude nanoparticle (NP) brain entry based on bulk brain analysis. Bulk brain includes blood, cerebrospinal fluid and blood vessels within the brain contributing to the blood–brain and blood–cerebrospinal fluid barriers. Considering the brain as neurons, glia and their extracellular space (brain parenchyma), most studies did not show brain parenchymal NP entry. Blood–brain and blood–cerebrospinal fluid barriers anatomy and function are reviewed. Methods demonstrating brain parenchymal NP entry are presented. Results demonstrating bulk brain versus brain parenchymal entry are classified. Studies are reviewed, critiqued and classified to illustrate results demonstrating bulk brain versus parenchymal entry. Brain, blood and peripheral organ NP timecourses are compared and related to brain parenchymal entry evidence suggesting brain NP timecourse informs about brain parenchymal entry.

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Henning, Erica C., Lawrence L. Latour, and Steven Warach. "Verification of Enhancement of the CSF Space, not Parenchyma, in Acute Stroke Patients with Early Blood—Brain Barrier Disruption." Journal of Cerebral Blood Flow & Metabolism 28, no. 5 (December 19, 2007): 882–86. http://dx.doi.org/10.1038/sj.jcbfm.9600598.

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Enhancement on post-contrast fluid-attenuated inversion recovery (FLAIR) images after acute stroke has been attributed to early blood—brain barrier disruption. Using an estimate of parenchymal volume fraction and the apparent diffusion coefficient (ADC), we investigated the relative contributions of cerebral spinal fluid (CSF) and parenchyma to enhancement seen on postcontrast FLAIR. Enhancing regions were found to have low parenchymal volume fractions and high ADC values, approaching that of pure CSF. These findings suggest that contrast enhancement on FLAIR occurs predominately in the CSF space, not parenchyma.

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Chowdhury, Forhad Hossain, Nur Mohammad, Mohammod Raziul Haque, Zahed Hossain, Md Abdus Salam, and Mainul Haque Sarker. "Tubercular Lesions in Brain Parenchyma." Bangladesh Journal of Infectious Diseases 5, no. 2 (July 11, 2019): 45–60. http://dx.doi.org/10.3329/bjid.v5i2.42151.

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Background: Preoperative neuro-radiological features of tuberculosis involving brain lesions may mimic neoplastic lesions of brain & skull base and post operative histopathological study or response to empirical anti-tubercular therapy brings the ultimate diagnosis. Objective: Here we present our experience of 76 cases of cerebral and cerebellar tuberculosis that was managed surgically with anti-tubercular drugs or medical treatment alone without histopathological confirmation. Methodology: All cases of brain parenchymal tuberculosis confirmed histopathologically after surgery or confirmed by succesfull conservative treatment with anti-TB from January 2008 to June 2015 were included for study. Tubercular meningitis was excluded from the study. Patients underwent some form of surgery that confirmed the tuberculosis by histopathologically. Patients with suspected tubercular lesion in brain were treated empirically with antiTB. Post operative imaging was done with CT scan of brain or MRI of brain in immediate post operative period, six months after operation and 18 months after operation. Results: 34 patients underwent surgery to confirm the tuberculosis and 44 patients with suspected tubercular lesion in brain were treated empirically with antiTB of which 40 patients responded successfully and rest 4 patients did not responded and underwent surgical excisional biopsy. Common clinical features include features of raised ICP with focal signs and symptoms. Concurrent other systemic tuberculosis was found in three cases. One patient had history of full course anti-tubercular therapy for pulmonary tuberculosis 20 years back. Conclusion: In suspected TB lesions, conservative treatment without histopathological diagnosis may be adopted with ultimate same result Bangladesh Journal of Infectious Diseases, December 2018;5(2):45-60

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Francisco, Allison De Freitas, Raul Fernando Pizzatto, Gustavo Henrique Smaniotto, Rodrigo Leite De Morais, Andrei Leite De Morais, and Ricardo Nascimento Brito. "Multiple Mieloma Metastases In Brain Parenchyma." JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 22, no. 3 (March 23, 2018): 124–27. http://dx.doi.org/10.22290/jbnc.v22i3.1021.

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Multiple myeloma in the central nervous system (CNS) is an extremely rare condition, described in over 100 cases in the literature. In this article, the authors report the case of a 55-year-old female patient, subjected to an autologous bonemarrow transplant, and, furthermore, to a brain tissue biopsy with immunohistochemistry confirmation, revealing infiltration by a great amount of plasma cells, compatible with the clinical history of multiple myeloma. The patient was then subjected to CNS adjuvant radiotherapy, with constant observation by clinical oncology and monthly pamidronate disodium prescription. Despite being an incurable pathology, radiation therapy showed important local control.

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Kosa, Gabor, Danilo De Lorenzo, Elena De Momi, Gabor Szekely, and Giancarlo Ferrigno. "Robotic burrowing in brain parenchyma tissue." IFAC Proceedings Volumes 44, no. 1 (January 2011): 14307–11. http://dx.doi.org/10.3182/20110828-6-it-1002.01840.

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Behnke, Stefanie, and G. Becker. "Sonographic imaging of the brain parenchyma." European Journal of Ultrasound 16, no. 1-2 (November 2002): 73–80. http://dx.doi.org/10.1016/s0929-8266(02)00039-3.

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Krumina, Gaida. "Metastatic disease of the brain: parenchyma." European Radiology 15, no. 3 (February 5, 2005): 608–16. http://dx.doi.org/10.1007/s00330-004-2626-4.

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Tabatabai, Ghazaleh, Joachim Baehring, and Fred H. Hochberg. "Primary Amyloidoma of the Brain Parenchyma." Archives of Neurology 62, no. 3 (March 1, 2005): 477. http://dx.doi.org/10.1001/archneur.62.3.477.

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Walter, Uwe, Christine Klein, Ruediger Hilker, Reiner Benecke, Peter P. Pramstaller, and Dirk Dressler. "Brain parenchyma sonography detects preclinical parkinsonism." Movement Disorders 19, no. 12 (2004): 1445–49. http://dx.doi.org/10.1002/mds.20232.

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Oh, Bryan C., Paul G. Pagnini, Michael Y. Wang, Charles Y. Liu, Paul E. Kim, Cheng Yu, and Michael L. J. Apuzzo. "STEREOTACTIC RADIOSURGERY: ADJACENT TISSUE INJURY AND RESPONSE AFTERHIGH-DOSE SINGLE FRACTION RADIATION." Neurosurgery 60, no. 1 (January 1, 2007): 31–45. http://dx.doi.org/10.1227/01.neu.0000249191.23162.d2.

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Abstract RADIOSURGERY IS NOW the preferred treatment modality for many intracranial disease processes. Although almost 50 years have passed since it was introduced as a tool to treat neurological disease, investigations into its effects on normal tissues of the central nervous system are still ongoing. The need for these continuing studies must be underscored. A fundamental understanding of the brain parenchymal response to radiosurgery would permit development of strategies that would enhance and potentiate the radiosurgical treatment effects on diseased tissue while mitigating injury to normal structures. To date, most studies on the response of the central nervous system to radiosurgery have been performed on brain tissue in the absence of pathological lesions, such as benign tumors or metastases. Although instructive, these investigations fail to emulate the majority of clinical scenarios that involve radiosurgical treatment of specific lesions surrounded by normal brain parenchyma. This article is the first in a two-part series that addresses the brain parenchyma's response to radiosurgery. This first article analyzes the histological, radiographic, and molecular data gathered regarding the brain parenchymal response to radiosurgery and aims to suggest future studies that could enhance our understanding of the topic. The second article in the series begins by discussing strategies for radiosurgical therapeutic enhancement. It concludes by focusing on strategies for mitigation and repair of radiation-induced brain injury.

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Brognaro, E. "P14.19 The inverse paradigm of IDH-wildtype glioblastoma is fundamental to overcome the two causes of resistance and develop novel effective therapies." Neuro-Oncology 21, Supplement_3 (August 2019): iii70. http://dx.doi.org/10.1093/neuonc/noz126.254.

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Abstract BACKGROUND IDH-wildtype glioblastoma behaves differently from all other solid tumors. This is the reason why after decades of praiseworthy therapeutic efforts, the prognosis remains very poor. Many clues (radiological, clinical, surgical) and recent indirect experimental evidence converge to indicate that the entire brain parenchyma is micro-infiltrated from the very beginning by the founding clone before the primary bulk has started its growth. Therefore, only in IDH-wildtype glioblastoma the malignant (i.e. distantly infiltrating the organ of origin) and deadly (leading cause to patient’s death) phases coincide and overlap in one single phase. MATERIALS AND METHODS Appropriate sampling procedures must absolutely take into consideration both the tumor bulk and the micro-infiltrated brain parenchyma. They can be performed (with full respect for ethical issues) analyzing neoplastic and “healthy” material obtained from living patients (a), using animal models (b), studying post-mortem samples from rapid autopsies (c), comparing local and distant recurrences with the primary bulk (d). The study and analysis of the bulk tumor must be carried out by collecting multiple multiregional spatially separated samples throughout the whole tumor mass. The analysis of the micro-infiltrated brain parenchyma in living patients can be performed appropriately and ethically also from surgical patient tissue. RESULTS The phylogenetic tree of the tumor bulk must be inferred and reconstructed by the collection and analysis of multiple regionally separated samples. Additionally, driver and passenger events will be identified as well as the CSCs of samples. The procedures to ethically sample the micro-infiltrated brain parenchyma enable us to collect and identify the founder CSCs which lie quiescent in the perivascular parenchymal niches across the whole brain. Indeed, distant recurrences are due to their activation. CONCLUSION IDH-wildtype glioblastoma is the only brain tumor which arises from astrocyte-like cells of the SVZ ribbon layer and it is able to micro-infiltrate the whole supratentorial brain parenchyma before starting its growth. Its unique inverse paradigm explains the emergence of distant recurrences (sharing only truncal mutations with the primary bulk) and adds, in addition to the heterogeneity of the primary bulk and its residues, a second crucial cause of resistance to take into account (i.e. the founder CSCs which reside quiescent, in G0 state, in the perivascular parenchymal niches). Therefore, innovative therapies must identify and selectively target either CSCs unique properties related to their impaired asymmetrical division or stable driver lesions of the founder CSC (without alternative mutations and pathways) or exclusive markers used by the founder CSCs to settle dormant (involving mechanisms of adhesion, anchorage and cell cycle arrest) in their niches.

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Alomran, B., D. Byrne, J. Walsh, N. Murray, F. Settecase, B. Rohr, and A. Rohr. "P.062 Does the intensity of brain parenchymal contrast staining on post-recanalization dual energy head CT (DECT) of stroke patients predict the fate of brain tissue?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (November 2021): S36. http://dx.doi.org/10.1017/cjn.2021.342.

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Background: On DECT, the ratio of maximum iodine concentration within parenchyma compared to the superior sagittal sinus has been shown to predict hemorrhagic transformation. We aimed to determine if this ratio also predicts the development of an infarct. Methods: 53 patients with small infarct cores (ASPECTS≥7) and good endovascular recanalization (mTICI 2b/3) were enrolled. Maximum brain parenchymal iodine concentration as per DECT relative to the superior sagittal sinus (iodine ratio) was correlated with the development of an infarct on follow up CT. Results: All patients showed contrast staining, 52 developed infarcts in the area of staining. The extent of infarction (smaller, equal or larger than area of staining) did not correlate with the iodine ratio. Conclusions: Brain parenchyma with contrast staining on post-procedure head CT almost invariably goes on to infarct, however the extent of infarct development is not predicted by the intensity of contrast staining. n=53 patients with successful recanalization of anterior circulation LVO infarct (TICI2b,3) with post procedural parenchymal iodine staining There was no correlation between the degree of contrast staining on initial post procedural CT as expressed in iodine ratio and F/U infarct extent.

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Lin, Baowan, Myron D. Ginsberg, Raul Busto, and Lin Li. "Hyperglycemic Transient Ischemia Induces Massive Neutrophil Deposition in Brain." Stroke 32, suppl_1 (January 2001): 353. http://dx.doi.org/10.1161/str.32.suppl_1.353-c.

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P80 Acute hyperglycemia worsens neurological signs and accentuates neuropathology after ischemia, but the mechanisms are poorly understood. In this study, we tested whether polymorphonuclear leukocytes (neutrophils) might be contributory. Anesthetized, physiologically monitored Wistar rats underwent global forebrain ischemia for 12.5 min by bilateral carotid artery occlusions plus hypotension (45 mm Hg). To induce hyperglycemia, rats received 2.5 ml of 25% dextrose i.p. 30 min prior to ischemia. Normoglycemic rats received saline. Plasma glucose levels were 340±66 and 133 ±21 mg/dl, respectively (mean±SD). Animals were sacrificed at either 24 h or 3 days by perfusion-fixation with FAM. Brain sections were reacted for the immunohistochemical visualization of myeloperoxidase (MPO), a specific and quantitative marker of neutrophil activity in the brain. In sham rats and in normoglycemic-ischemic animals, almost no MPO-positive cells were identified. In marked contrast, brains of hyperglycemic-ischemic rats studied at 24 h contained dramatic accumulations of MPO-positive cells within pial and parenchymal blood vessels as well as within cortical and subcortical parenchyma. MPO-positivity was most robust in areas of severe injury (on H&E sections), but MPO cells were also observed in areas without overt injury. Intravascular MPO-positive cells commonly obstructed the vascular lumen. Following 3-d survival, MPO-positivity of hyperglycemic-ischemic brains had significantly decreased. In hyperglycemic brains studied at 24 h, median numbers of MPO-positive cells were increased by 130-fold in cortex and 110-fold in striatum above values in normoglycemic-ischemic rats. In summary, this study shows that preischemic hyperglycemia triggers the early and dramatic deposition of polymorphonuclear leukocytes in the postischemic brain, with neutrophil adherence to cerebral blood vessels and their migration into brain parenchyma following brief forebrain ischemia. These events may contribute to the enhanced tissue destruction, extension of infarction, and BBB disruption observed in hyperglycemic ischemia. Supported by NIH Grant NS05820.

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Babicsak, Viviam R., Adriana V. Klein, Miriam H. Tsunemi, and Luiz C. Vulcano. "Brain parenchymal changes during normal aging in domestic cats." Pesquisa Veterinária Brasileira 38, no. 6 (June 2018): 1196–202. http://dx.doi.org/10.1590/1678-5150-pvb-5397.

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ABSTRACT: This study aimed to identify changes related to brain parenchyma as advancing age in healthy domestic cats. Our hypothesis is that cats suffer cerebral and cerebellar atrophy and show focal changes in signal intensity of the brain parenchyma in accordance with the progression of age. Twelve adult (1 to 6 years), eleven mature (7 to11 years) and ten geriatric non-brachycephalic cats (12 years or more of age) underwent brain magnetic resonance imaging (MRI). There were no changes in signal intensity and contrast uptake in brain parenchyma of the cats. Geriatric animals showed significantly lower average thickness of the interthalamic adhesion and percentage of the cerebral parenchyma volume in relation to intracranial volume than those found in the adult group. No significant differences were found between groups for cerebral volume, cerebellar volume and percentage of cerebellar volume in relation to intracranial volume. The results of this study indicate that atrophy of the cerebral parenchyma, including the interthalamic adhesion, occurs with age in domestic cats, confirming the hypothesis of the study. However, the results did not corroborate the hypothesis that cats show cerebellar atrophy and focal changes in signal intensity of the brain parenchyma with advancing age.

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Hafeez, Moiz, and Nazir Khan. "DWI and NCCT - Ischemic patterns in global anoxic brain injury." IP Indian Journal of Neurosciences 7, no. 3 (September 15, 2021): 251–53. http://dx.doi.org/10.18231/j.ijn.2021.045.

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This case report highlights differences between diffusion weighted imaging (DWI) and computed tomography (CT) with respect to the extent of ischemic changes detectable in brain parenchyma during global anoxic brain injury. Brain CT in a 65 year old patient post cardiac arrest showed striking diffuse loss of Gray-White matter differentiation consistent with global anoxic brain injury while magnetic resonance imaging (MRI) performed 3 days later showed diffusion restriction and hyperintensity only in select areas. DWI hyperintensity was seen in diverse structures including the hippocampi, globus pallidus, forniceal columns, medial occipital lobes as well as the left amygdala. Although generally presumed to be the most sensitive modality for detecting parenchymal ischemia, this case demonstrates that CT may sometimes better capture the extent of parenchymal damage during anoxic brain injury.

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Yamamoto, Junkoh, Shingo Kakeda, Yukunori Korogi, Takeshi Saito, and Yoshiteru Nakano. "MET-04 EVALUATION OF PERITUMORAL BRAIN PARENCHYMA USING CONTRAST-ENHANCED FIESTA IMAGING FOR DIFFERENTIATING METASTATIC BRAIN TUMORS AND GLIOBLASTOMAS." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii35. http://dx.doi.org/10.1093/noajnl/vdz039.159.

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Abstract Introduction: Metastatic brain tumors and glioblastomas commonly revealed heterogenous enhancement lesions with peritumoral brain edema on magnetic resonance imaging (MRI). In particular, distinguishing solitary metastatic brain tumors from glioblastomas is difficult on conventional MRI. Fast imaging employing steady-state acquisition (FIESTA) can emphasize the water content signal with a high spatial resolution. In this study, we evaluate a role of contrast-enhanced FIESTA(CE-FIESTA) by focusing on the peritumoral brain parenchyma between metastatic brain tumors and glioblastomas. Materials and Methods: We included patients who underwent initial surgery and were histologically diagnosed with metastatic brain tumor (43 cases) or glioblastoma (14 cases) between November 2008 and May 2016. We evaluated CE-FIESTA findings of peritumoral brain parenchyma. Next, we performed an observer performance study with neuroradiologists based on the findings of peritumoral brain parenchyma using conventional MRI and CE-FIESTA. Results: CE-FIESTA revealed hyperintense rim in peritumoral brain parenchyma. We classified hyperintense rim in three groups, as follow: type A, no hyperintense rim; type B, partial hyperintense rim; and type C, extended hyperintense rim. Regarding the diagnosis of metastatic brain tumors, the observer performance demonstrated high sensitivity (95.3%), specificity (85.7%) and accuracy (93.0%) of type C on CE-FIESTA, and thus, CE-FIESTA could distinguish metastatic brain tumors from glioblastomas with high accuracy. Conclusions: CE-FIESTA may provide useful information for distinguish metastatic brain tumors from glioblastomas, focusing on the differences in the peritumoral brain parenchyma.

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Amans, Matthew R., Daniel L. Cooke, Maya Vella, Christopher F. Dowd, Van V. Halbach, Randall T. Higashida, and Steven W. Hetts. "Contrast Staining on CT after DSA in Ischemic Stroke Patients Progresses to Infarction and Rarely Hemorrhages." Interventional Neuroradiology 20, no. 1 (January 2014): 106–15. http://dx.doi.org/10.15274/inr-2014-10016.

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Contrast staining of brain parenchyma identified on non-contrast CT performed after DSA in patients with acute ischemic stroke (AIS) is an incompletely understood imaging finding. We hypothesize contrast staining to be an indicator of brain injury and suspect the fate of involved parenchyma to be cerebral infarction. Seventeen years of AIS data were retrospectively analyzed for contrast staining. Charts were reviewed and outcomes of the stained parenchyma were identified on subsequent CT and MRI. Thirty-six of 67 patients meeting inclusion criteria (53.7%) had contrast staining on CT obtained within 72 hours after DSA. Brain parenchyma with contrast staining in patients with AIS most often evolved into cerebral infarction (81%). Hemorrhagic transformation was less likely in cases with staining compared with hemorrhagic transformation in the cohort that did not have contrast staining of the parenchyma on post DSA CT (6% versus 25%, respectively, OR 0.17, 95% CI 0.017–0.98, p = 0.02). Brain parenchyma with contrast staining on CT after DSA in AIS patients was likely to infarct and unlikely to hemorrhage.

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Sundgren, Pia C., and Yue Cao. "Brain Irradiation: Effects on Normal Brain Parenchyma and Radiation Injury." Neuroimaging Clinics of North America 19, no. 4 (November 2009): 657–68. http://dx.doi.org/10.1016/j.nic.2009.08.014.

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Kohandel, M., S. Sivaloganathan, G. Tenti, and J. M. Drake. "The constitutive properties of the brain parenchyma." Medical Engineering & Physics 28, no. 5 (June 2006): 449–54. http://dx.doi.org/10.1016/j.medengphy.2005.01.005.

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Alliot, F., J. Rutin, P. J. M. Leenen, and B. Pessac. "Brain parenchyma vessels and the angiotensin system." Brain Research 830, no. 1 (May 1999): 101–12. http://dx.doi.org/10.1016/s0006-8993(99)01373-6.

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Andescavage, Nickie N., Adre DuPlessis, Robert McCarter, Gilbert Vezina, Richard Robertson, and Catherine Limperopoulos. "Cerebrospinal Fluid and Parenchymal Brain Development and Growth in the Healthy Fetus." Developmental Neuroscience 38, no. 6 (2016): 420–29. http://dx.doi.org/10.1159/000456711.

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Objective: The objective of this study was to apply quantitative magnetic resonance imaging to characterize absolute cerebrospinal fluid (CSF) development, as well as its relative development to fetal brain parenchyma in the healthy human fetus. Design: We created three-dimensional high-resolution reconstructions of the developing brain for healthy fetuses between 18 and 40 weeks' gestation, segmented the parenchymal and CSF spaces, and calculated the volumes for the lateral, third, and fourth ventricles; extra-axial CSF space; and the cerebrum, cerebellum, and brainstem. From these data, we constructed normograms of the resulting volumes according to gestational age and described the relative development of CSF to fetal brain parenchyma. Results: Each CSF space demonstrated major increases in volumetric growth during the second half of gestation: third ventricle (23-fold), extra-axial CSF (11-fold), fourth ventricle (8-fold), and lateral ventricle (2-fold). Total CSF volume was related to total brain volume (p < 0.01), as was lateral ventricle to cerebral volume (p < 0.01); however, the fourth ventricle was not related to cerebellar or brainstem volume (p = 0.18-0.19). Relevance: Abnormalities of the CSF spaces are the most common anomalies of neurologic development detected on fetal screening using neurosonography. Normative values of absolute CSF volume, as well as relative growth in comparison to intracranial parenchyma, provide valuable insight into normal fetal neurodevelopment. These data may provide important biomarkers of early deviations from normal growth, better distinguish between benign variants and early disease, and serve as reference standards for postnatal growth and development in the premature infant.

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Kinjo, Ichiko, Denis E. Bragin, and Bridget S. Wilson. "Dissecting the mechanisms underling acute lymphoblastic leukemia brain metastasis." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 50.5. http://dx.doi.org/10.4049/jimmunol.196.supp.50.5.

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Abstract Despite improved treatments, patient with B-cell precursor acute lymphoblastic leukemia (BCP-ALL) experience relapse with devastating tumor cell dissemination into the central nervous system (CNS). As an “immune privilege site”, CNS is protected from infiltration of immune cells by specialized structure of blood-brain barrier with astrocyte endfeet that surround the blood vessels. To assess whether leukemia cells hijack mechanisms employed by inflamed immune cells to invade into the brain parenchyma, we set up leukemia mouse xenograft models with well-characterized human BCP-ALL cell lines and primary cells derived from patients. We found massive infiltration/colonization of GFP+ leukemia cells inside brain vessels and parenchyma addition to meningeal space. Immunohistochemistry staining showed that activation of astrocytes following the induction of VEGF-A in brains of leukemia burden mice. We address phenotype changes in leukemia cells, that are associated with brain metastasis by comparing the expression of chemokine receptors and cytokines in leukemia cells recovered from bone marrow and other extramedullary sites (spleen, liver) for comparison to the cells recovered from brain tissue. By investigation of extravasation steps in intact brain, we also try to figure how leukemia cells bleach the BBB and find new niche to colonize at brain parenchyma. Ongoing studies will provide new insights into the mechanisms that regulate leukemia CNS infiltration.

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Paris, Justine, Eurydice Angeli, and Guilhem Bousquet. "The Pharmacology of Xenobiotics after Intracerebro Spinal Fluid Administration: Implications for the Treatment of Brain Tumors." International Journal of Molecular Sciences 22, no. 3 (January 28, 2021): 1281. http://dx.doi.org/10.3390/ijms22031281.

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The incidence of brain metastasis has been increasing for 10 years, with poor prognosis, unlike the improvement in survival for extracranial tumor localizations. Since recent advances in molecular biology and the development of specific molecular targets, knowledge of the brain distribution of drugs has become a pharmaceutical challenge. Most anticancer drugs fail to cross the blood–brain barrier. In order to get around this problem and penetrate the brain parenchyma, the use of intrathecal administration has been developed, but the mechanisms governing drug distribution from the cerebrospinal fluid to the brain parenchyma are poorly understood. Thus, in this review we discuss the pharmacokinetics of drugs after intrathecal administration, their penetration of the brain parenchyma and the different systems causing their efflux from the brain to the blood.

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Shellikeri, Sphoorti, Harrison Bai, Randolph M. Setser, Robert W. Hurst, and Anne Marie Cahill. "Association of intracranial arteriovenous malformation embolization with more rapid rate of perfusion in the peri-nidal region on color-coded quantitative digital subtraction angiography." Journal of NeuroInterventional Surgery 12, no. 9 (March 18, 2020): 902–5. http://dx.doi.org/10.1136/neurintsurg-2019-015776.

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BackgroundHemodynamic alterations post-embolization of intracranial arteriovenous malformations (AVMs) may cause delayed edema/hemorrhage in brain parenchyma adjacent to the lesion.ObjectiveTo quantify and compare cerebral perfusion changes in the peri-AVM territory pre- and post-embolization using color-coded quantitative digital subtraction angiography (q-DSA).MethodsPediatric intracranial AVM embolization procedures performed over a 5 year period were included. DSA images of all patients were retrospectively assessed using syngo iFlow. Regions of interest (ROI) were selected on anteroposterior and lateral q-DSA views: three in the peri-AVM region; two in parenchyma distant from the AVM. Time-to-peak (TTP) contrast enhancement of ROIs and ∆TTP (TTP at the selected ROI minus TTP at either the ipsilateral internal carotid/vertebral artery) were measured.Result19 pediatric patients with 19 AVMs (9 males/10 females, mean age 12 years) underwent intracranial AVM embolization: 15/19 AVMs were supplied by the anterior circulation and 4/19 by the posterior circulation. Blood flow was significantly slower post-embolization in the draining vein (19/19) (p<0.01), and the venous sinus outflow (17/19) (p<0.01), by mean difference of 2.01±1.31 s and 1.74±2.04 s. There was significantly increased peri-AVM parenchymal perfusion post-embolization (∆TTP=2.20±0.48 s) compared with pre-embolization (∆TTP=2.52±0.42 s), by an average ∆TTP of 0.33±0.53 s (p=0.014). In contrast, there was no perfusion difference (∆TTP=0.03±0.20 s, p=0.8) between pre- and post-embolization in the distant parenchyma. The size of the AVM was not correlated with change in peri-nidal parenchymal perfusion (r=−0.136, p=0.579).ConclusionThis study demonstrates more rapid perfusion in the peri-nidal brain parenchyma post-embolization of the AVM, which supports the theory that increased perfusion in normal tissue surrounding the AVM after embolization may underlie some post-procedural complications.

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Bernardes-Silva, Martine, Daniel C. Anthony, Andrew C. Issekutz, and V. Hugh Perry. "Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins." Journal of Cerebral Blood Flow & Metabolism 21, no. 9 (September 2001): 1115–24. http://dx.doi.org/10.1097/00004647-200109000-00009.

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The adult central nervous system parenchyma is resistant to inflammation, but in juvenile rats the injection of inflammatory mediators, interleukin-1β for example, gives rise to extensive neutrophil recruitment and neutrophil-dependent blood–brain barrier breakdown. The factors that confer this resistant phenotype are unknown. In this study, the authors demonstrate that E- and P-selectin expression is increased to a similar extent in adult and juvenile brain after the intracerebral injection of IL-1β. Thus, the refractory nature of the brain parenchyma cannot be attributed to an absence of selectin expression. However, in injuries where the resistant characteristic of the brain parenchyma is compromised, and neutrophil recruitment occurs, selectin blockade may be an advantage. The authors investigated the contribution that selectins make to neutrophil recruitment during acute inflammation in the brain. The authors examined neutrophil recruitment by immunohistochemistry on brain sections of juvenile rats killed four hours after the intracerebral injection of IL-1β and the intravenous injection of neutralizing anti-selectin monoclonal antibodies (mAb). The administration of the P-selectin blocking mAb inhibited neutrophil recruitment by 85% compared with controls. Surprisingly, E-selectin blockade had no effect on neutrophil recruitment to the brain parenchyma. Thus, P-selectin appears to play a pivotal role in mediating neutrophil recruitment to the brain parenchyma during acute inflammation.

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Kulcsár, Zsolt, Paolo Machi, Maria Isabel Vargas, Karl Schaller, and Karl Olof Lovblad. "Single-hole, ruptured parenchymal arteriovenous fistula of the mesencephalon : Not known vascular malformation of the brain or a posthemorrhagic entity?" Ideggyógyászati szemle 74, no. 3-4 (2021): 126–28. http://dx.doi.org/10.18071/isz.74.0126.

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The subtypes of brain arteriovenous malformations, with direct, single-hole fistulas without co-existing nidus are not described as existing entities inside the brain parenchyma but on the pial surface. True parenchymal arteriovenous malformations present with nidal structure, even if they are small, whereas surface lesions may present a direct fistulous configuration. In this case of midbrain haemorrhage a direct arteriovenous fistula was detected at the level of the red nucleus between a paramedian midbrain perforator artery and a paramedian parenchymal vein, with pseudo-aneurysm formation at the fistulous connection, without signs of adjacent nidus structure. The hypothesis whether a pre-existing arteriovenous fistula ruptured or a spontaneous haemorrhage has caused the fistulous connection is discussed.

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Cruz-Orengo, Lillian, David W. Holman, Denise Dorsey, Liang Zhou, Penglie Zhang, Melissa Wright, Erin E. McCandless, et al. "CXCR7 influences leukocyte entry into the CNS parenchyma by controlling abluminal CXCL12 abundance during autoimmunity." Journal of Experimental Medicine 208, no. 2 (February 7, 2011): 327–39. http://dx.doi.org/10.1084/jem.20102010.

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Loss of CXCL12, a leukocyte localizing cue, from abluminal surfaces of the blood–brain barrier occurs in multiple sclerosis (MS) lesions. However, the mechanisms and consequences of reduced abluminal CXCL12 abundance remain unclear. Here, we show that activation of CXCR7, which scavenges CXCL12, is essential for leukocyte entry via endothelial barriers into the central nervous system (CNS) parenchyma during experimental autoimmune encephalomyelitis (EAE), a model for MS. CXCR7 expression on endothelial barriers increased during EAE at sites of inflammatory infiltration. Treatment with a CXCR7 antagonist ameliorated EAE, reduced leukocyte infiltration into the CNS parenchyma and parenchymal VCAM-1 expression, and increased abluminal levels of CXCL12. Interleukin 17 and interleukin 1β increased, whereas interferon-γ decreased, CXCR7 expression on and CXCL12 internalization in primary brain endothelial cells in vitro. These findings identify molecular requirements for the transvascular entry of leukocytes into the CNS and suggest that CXCR7 blockade may have therapeutic utility for the treatment of MS.

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Brahimaj, Bledi, Michael Lamba, John C. Breneman, and Ronald E. Warnick. "Iodine-125 seed migration within brain parenchyma after brachytherapy for brain metastasis: case report." Journal of Neurosurgery 125, no. 5 (November 2016): 1167–70. http://dx.doi.org/10.3171/2015.11.jns151464.

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This case report documents the migration of 3 iodine-125 (125I) seeds from the tumor resection cavity into brain parenchyma over a 7-year period. A 66-year-old woman had a history of metastatic ovarian carcinoma, nickel allergy, and reaction to a titanium hip implant that required reoperation for hardware removal. In this unique case of parenchymal migration, the seed paths seemed to follow white matter tracts, traveling between 18.5 and 35.5 mm from the initial implant site. The patient's initial neurological decline, which was thought to be related to radiation necrosis, appeared to stabilize with medical therapy. She subsequently developed progressive right hemispheric edema that resulted in neurological deterioration and death. Considering her previous reactions to nickel and titanium, the authors now speculate that her later clinical course reflected an allergic reaction to the titanium casing of the 125I seeds. Containing a trace amount of nickel, 125I seeds can elicit a delayed hypersensitivity reaction in patients with a history of nickel dermatitis. Preoperative patch testing is recommended in these patients, and 125I seed implantation should be avoided in those who test positive.

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Sulistyo, Eko, and Ildsa Maulidya Mar’athus N. "DIFFERENCE IMPLEMENTATION OF T1WI SE AND T1WI FSPGR BRAVO SEQUENTS IN MRI BRAIN TUMOR." Journal of Applied Health Management and Technology 1, no. 1 (October 8, 2019): 23–27. http://dx.doi.org/10.31983/jahmt.v1i1.5307.

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Tumor is basically an uncontrolled growth of cancerous cells in any part of the body, whereas a brain tumor is an uncontrolled growth of cancerous cells in the brain. Useing of MRI in diagnose tumors can be done with various sequences. Contrast medium is needed to evince tumor enhancement, as well as sequences that support to produce tumor in post contrast, one of which uses a conventional sequence T1WI SE. This sequences often lose information in providing images in cases of brain tumors and generally more time consuming. FSPGR BRAVO is a 3D volumetric acquisition that captures thin section images with near isotropic or isotropic spatial resolution. This sequence displays anatomy, especially brain parenchymal anatomy, in fine detail. The type of research in this mini research is a qualitative study with an observational approach which aims to find out sequences that can optimize post-MRI images in contrast to brain tumor cases with a short time and get the right diagnosis. Convensional sequence of MRI TIWI SE can’t detection of lessions in cerebral cortex. FSPGR BRAVO in producing images in 3D format in one-time retrieval of one particular piece and able to display anatomy especially the anatomy of the brain parenchyma in fine detail. FSPGR BRAVO can be used to assist cause to be uprise the diagnosis of MRI brain tumor by displaying the anatomy of the brain parenchyma in more fine detail, without the need for extended time.

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Doolittle, Nancy D., Lauren Abrey, Tamara Shenkier, Tali Siegal, Jacoline Bromberg, Edward Neuwelt, Carole Soussain, et al. "Isolated Brain Parenchyma Relapse of Non-Hodgkin’s Lymphoma (NHL): A Descriptive Analysis from the International Primary CNS Lymphoma Collaborative Group (IPCG)." Blood 108, no. 11 (November 1, 2006): 2026. http://dx.doi.org/10.1182/blood.v108.11.2026.2026.

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Abstract Background: Isolated brain parenchyma relapse as initial site of relapse is a rare complication of NHL and carries a poor prognosis. Few large series focus on treatment characteristics and outcomes of isolated brain parenchyma relapse of NHL. Methods: The IPCG conducted a retrospective review of patient and treatment characteristics and outcomes of this complication. Following initial diagnosis and treatment of NHL (1980–2004), cases with brain parenchyma relapse as initial relapse site, with no evidence of lymphoma elsewhere in the body at the time of brain relapse, were eligible. Cases with brain, spine or leptomeningeal involvement at NHL diagnosis were not eligible. Results: 113 cases were assembled from 13 investigators in 8 countries. Preliminary data summaries are: 94 (83%) cases had diffuse large B-cell NHL, 5 (4%) follicular lymphoma, 3 (3%) Burkitt’s lymphoma, other NHL subtypes (11) . Median age at NHL diagnosis was 61yrs (16–85 yrs). 55% were male. Median ECOG at NHL diagnosis was 1. Median time from NHL diagnosis to isolated brain relapse was 1.8 yrs (3 months–15.9 yrs). 76 (67%) relapsed in brain less than 3 yrs after NHL diagnosis. Symptoms at brain relapse included mental status changes in 37%, gait/balance disturbance (27%), motor/sensory symptoms (23%). Median ECOG at brain relapse was 2. Parenchyma relapse was documented by brain imaging plus biopsy in 54 (48%), or imaging without biopsy in 58 (52%); not reported (1). 53 (48%) cases had one brain lesion; 56 (50%) had two or more lesions; not reported (4). Site of relapse was cerebral hemispheres in 53 (48%) cases, deep brain structures (brain stem/cerebellum) in 30 (27%), cerebral hemispheres and deep brain structures in 23 (21%); not reported (7). At brain relapse, CSF was positive in 11 (10%) cases, negative in 56 (50%); not reported (46[40%]). Treatment for brain relapse was chemotherapy alone in 52 (46%) cases, WBRT alone in 34 (30%), chemotherapy followed by RT in 26 (23%), and brain surgery alone (1). 78 (69%) cases are deceased. Median survival from brain parenchyma relapse to death was 1.6 yrs (95% CI: 11 months–2.6 yrs). Effect of treatment type at brain relapse on survival, will be reported. Brain lymphoma was the cause of death in 49 (63%) cases; CNS toxicity was the cause in 6 (8%) cases. Conclusion: Though a rare relapse site, prospective studies are needed to improve understanding and outcomes of isolated brain parenchyma relapse of NHL.

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Bonfanti, Luca. "The (Real) Neurogenic/Gliogenic Potential of the Postnatal and Adult Brain Parenchyma." ISRN Neuroscience 2013 (February 6, 2013): 1–14. http://dx.doi.org/10.1155/2013/354136.

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During the last two decades basic research in neuroscience has remarkably expanded due to the discovery of neural stem cells (NSCs) and adult neurogenesis in the mammalian central nervous system (CNS). The existence of such unexpected plasticity triggered hopes for alternative approaches to brain repair, yet deeper investigation showed that constitutive mammalian neurogenesis is restricted to two small “neurogenic sites” hosting NSCs as remnants of embryonic germinal layers and subserving homeostatic roles in specific neural systems. The fact that in other classes of vertebrates adult neurogenesis is widespread in the CNS and useful for brain repair sometimes creates misunderstandings about the real reparative potential in mammals. Nevertheless, in the mammalian CNS parenchyma, which is commonly considered as “nonneurogenic,” some processes of gliogenesis and, to a lesser extent, neurogenesis also occur. This “parenchymal” cell genesis is highly heterogeneous as to the position, identity, and fate of the progenitors. In addition, even the regional outcomes are different. In this paper the heterogeneity of mammalian parenchymal neurogliogenesis will be addressed, also discussing the most common pitfalls and misunderstandings of this growing and promising research field.

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Sangha, Vishal, Md Tozammel Hoque, Jeffrey Henderson, and Reina Bendayan. "Localization of the Folate Transport Systems in the Murine Central Nervous System." Current Developments in Nutrition 5, Supplement_2 (June 2021): 922. http://dx.doi.org/10.1093/cdn/nzab049_035.

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Abstract Objectives Folates are critical for normal neurodevelopment, and folate transport in the brain is primarily mediated by folate receptor alpha (FRα) at the blood-cerebrospinal fluid barrier (BCSFB). However, studies have reported folate transporter/receptor expression in other brain compartments, which may significantly contribute to overall brain folate uptake. The objective of this study is to characterize the localization of the folate transport systems i.e., reduced folate carrier (RFC), proton-coupled folate transporter (PCFT), and FRα in the mouse central nervous system, which will provide insight on novel routes of brain folate transport. In particular, folate transporter/receptor localization is examined at brain barriers [blood-brain barrier (BBB), BCSFB, arachnoid barrier (AB)] and in brain parenchyma (astrocytes, microglia, neurons). Methods The localization of RFC, PCFT and FRα was observed in the brains of C57BL6/N wildtype mice by applying immunohistochemistry (IHC). Mouse brains were isolated, and IHC was performed on frozen coronal sections. Transporter/receptor localization was examined at brain barriers (BBB, BCSFB, AB) and in brain parenchyma (astrocytes, neurons, microglia) using specific antibodies. Standard IHC markers were utilized to identify various brain compartments, with confocal microscopy used for imaging. Results At the mouse BBB and BCSFB, localization of RFC, PCFT and FRα was observed, which is consistent with previous reported data and our own work. At the AB, in astrocytes and neurons localization of RFC and PCFT (but not FRα) was observed. In microglia, no expression of the folate transporters or receptor was detected. Conclusions RFC and PCFT localization at the AB may represent a novel route of folate transport into the CSF, with transporter expression in neurons and astrocytes facilitating folate uptake into brain parenchyma cellular targets. Modulating folate transport at these brain compartments may provide a novel strategy in increasing brain folate uptake in disorders associated with defective FRα and impaired brain folate transport at the BCSFB. Funding Sources This work is supported by the Natural Sciences and Engineering Research Council of Canada (RB). VS is a recipient of several graduate scholarships.

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Stevenson, P. G., J. M. Austyn, and S. Hawke. "Uncoupling of virus-induced inflammation and anti-viral immunity in the brain parenchyma." Journal of General Virology 83, no. 7 (July 1, 2002): 1735–43. http://dx.doi.org/10.1099/0022-1317-83-7-1735.

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Non-neuroadapted influenza virus confined to the brain parenchyma does not induce antigen-specific immunity. Nevertheless, infection in this site upregulated major histocompatibility complex (MHC) class I and MHC class II expression and recruited lymphocytes to a perivascular compartment. T cells recovered from the brain had an activated/memory phenotype but did not respond to viral antigens. In contrast, T cells recovered from the brain after infection in a lateral cerebral ventricle, which is immunogenic, showed virus-specific responses. As with infectious virus, influenza virus-infected dendritic cells elicited virus-specific immunity when inoculated into the cerebrospinal fluid but not when inoculated into the brain parenchyma. Thus, inflammation and dendritic cell function were both uncoupled from immune priming in the microenvironment of the brain parenchyma and neither was sufficient to overcome immunological privilege.

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Gurevitz, Stacy A., Justin M. Goldfarb, Barry Cooper, John R. Krause, and Marvin J. Stone. "Biopsy-Proven Mantle Cell Lymphoma in Brain Parenchyma." Baylor University Medical Center Proceedings 24, no. 1 (January 2011): 45–47. http://dx.doi.org/10.1080/08998280.2011.11928681.

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ATSUMI, Noritoshi, Satoko HIRABAYASHI, Eiichi TANAKA, and Masami IWAMOTO. "537 Modeling of Mechanical Properties of Brain Parenchyma." Proceedings of Conference of Tokai Branch 2013.62 (2013): 333–34. http://dx.doi.org/10.1299/jsmetokai.2013.62.333.

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Frevert, Ute, Alexandru Movila, Olga V. Nikolskaia, Jayne Raper, Zachary B. Mackey, Maha Abdulla, James McKerrow, and Dennis J. Grab. "Early Invasion of Brain Parenchyma by African Trypanosomes." PLoS ONE 7, no. 8 (August 31, 2012): e43913. http://dx.doi.org/10.1371/journal.pone.0043913.

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Gorukhina, O. A., R. D. Ilyuk, and I. V. Mishchenko. "Accumulation of exogenous histone in rat brain parenchyma." Bulletin of Experimental Biology and Medicine 130, no. 1 (July 2000): 665–68. http://dx.doi.org/10.1007/bf02682100.

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Sanavio, Barbara, Laura Librizzi, Paolo Pennacchio, Galina V. Beznoussenko, Fernanda Sousa, Paulo Jacob Silva, Alexander A. Mironov, et al. "Distribution of superparamagnetic Au/Fe nanoparticles in an isolated guinea pig brain with an intact blood brain barrier." Nanoscale 10, no. 47 (2018): 22420–28. http://dx.doi.org/10.1039/c8nr07182a.

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Spellerberg, B., S. Prasad, C. Cabellos, M. Burroughs, P. Cahill, and E. Tuomanen. "Penetration of the blood-brain barrier: enhancement of drug delivery and imaging by bacterial glycopeptides." Journal of Experimental Medicine 182, no. 4 (October 1, 1995): 1037–43. http://dx.doi.org/10.1084/jem.182.4.1037.

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The blood-brain barrier restricts the passage of many pharmacological agents into the brain parenchyma. Bacterial glycopeptides induce enhanced blood-brain barrier permeability when they are present in the subarachnoid space during meningitis. By presenting such glycopeptides intravenously, blood-brain barrier permeability in rabbits was enhanced in a reversible time- and dose-dependent manner to agents < or = 20 kD in size. Therapeutic application of this bioactivity was evident as enhanced penetration of the antibiotic penicillin and the magnetic resonance imaging contrast agent gadolinium-diethylene-triamine-pentaacetic acid into the brain parenchyma.

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Crooks, Elliot J., Brandon A. Irizarry, Martine Ziliox, Toru Kawakami, Tiffany Victor, Feng Xu, Hironobu Hojo, et al. "Copper stabilizes antiparallel β-sheet fibrils of the amyloid β40 (Aβ40)-Iowa variant." Journal of Biological Chemistry 295, no. 27 (May 6, 2020): 8914–27. http://dx.doi.org/10.1074/jbc.ra119.011955.

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Cerebral amyloid angiopathy (CAA) is a vascular disorder that primarily involves deposition of the 40-residue–long β-amyloid peptide (Aβ40) in and along small blood vessels of the brain. CAA is often associated with Alzheimer's disease (AD), which is characterized by amyloid plaques in the brain parenchyma enriched in the Aβ42 peptide. Several recent studies have suggested a structural origin that underlies the differences between the vascular amyloid deposits in CAA and the parenchymal plaques in AD. We previously have found that amyloid fibrils in vascular amyloid contain antiparallel β-sheet, whereas previous studies by other researchers have reported parallel β-sheet in fibrils from parenchymal amyloid. Using X-ray fluorescence microscopy, here we found that copper strongly co-localizes with vascular amyloid in human sporadic CAA and familial Iowa-type CAA brains compared with control brain blood vessels lacking amyloid deposits. We show that binding of Cu(II) ions to antiparallel fibrils can block the conversion of these fibrils to the more stable parallel, in-register conformation and enhances their ability to serve as templates for seeded growth. These results provide an explanation for how thermodynamically less stable antiparallel fibrils may form amyloid in or on cerebral vessels by using Cu(II) as a structural cofactor.

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Huang, Jianpan, Peter C. M. van Zijl, Xiongqi Han, Celia M. Dong, Gerald W. Y. Cheng, Kai-Hei Tse, Linda Knutsson, et al. "Altered d-glucose in brain parenchyma and cerebrospinal fluid of early Alzheimer’s disease detected by dynamic glucose-enhanced MRI." Science Advances 6, no. 20 (May 2020): eaba3884. http://dx.doi.org/10.1126/sciadv.aba3884.

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Altered cerebral glucose uptake is one of the hallmarks of Alzheimer’s disease (AD). A dynamic glucose-enhanced (DGE) magnetic resonance imaging (MRI) approach was developed to simultaneously monitor d-glucose uptake and clearance in both brain parenchyma and cerebrospinal fluid (CSF). We observed substantially higher uptake in parenchyma of young (6 months) transgenic AD mice compared to age-matched wild-type (WT) mice. Notably lower uptakes were observed in parenchyma and CSF of old (16 months) AD mice. Both young and old AD mice had an obviously slower CSF clearance than age-matched WT mice. This resembles recent reports of the hampered CSF clearance that leads to protein accumulation in the brain. These findings suggest that DGE MRI can identify altered glucose uptake and clearance in young AD mice upon the emergence of amyloid plaques. DGE MRI of brain parenchyma and CSF has potential for early AD stratification, especially at 3T clinical field strength MRI.

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Stevenson, P. G., S. Freeman, C. R. Bangham, and S. Hawke. "Virus dissemination through the brain parenchyma without immunologic control." Journal of Immunology 159, no. 4 (August 15, 1997): 1876–84. http://dx.doi.org/10.4049/jimmunol.159.4.1876.

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Abstract After inoculation into the cerebrospinal fluid, the neurovirulent influenza virus A/WSN caused a rapidly progressive encephalitis that was uniformly fatal within 8 days. After inoculation into the brain parenchyma, the same virus replicated for 7 to 20 days without causing clinical illness, but when infection reached the cerebrospinal fluid, encephalitis was lethal within a further 6 days. As the virus spread through the brain parenchyma, there was intense intracerebral inflammation, with up-regulation of MHC class I and MHC class II expression and recruitment of CD44(high) CD49d(high) T cells. However, this was not associated with antiviral Ab production, and the infiltrating cells, unlike primed A/WSN-specific T cells, did not eliminate the virus in vivo or show evidence of virus recognition in vitro. Thus, a neurovirulent virus was able to disseminate widely through the brain parenchyma and induce considerable intracerebral inflammation without eliciting protective immunity.

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Parodi-Rullán, Rebecca M., Sabzali Javadov, and Silvia Fossati. "Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease." Cells 10, no. 11 (October 27, 2021): 2903. http://dx.doi.org/10.3390/cells10112903.

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Alzheimer’s disease (AD) is the most prevalent cause of dementia and is pathologically characterized by the presence of parenchymal senile plaques composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles of hyperphosphorylated tau protein. The accumulation of Aβ also occurs within the cerebral vasculature in over 80% of AD patients and in non-demented individuals, a condition called cerebral amyloid angiopathy (CAA). The development of CAA is associated with neurovascular dysfunction, blood–brain barrier (BBB) leakage, and persistent vascular- and neuro-inflammation, eventually leading to neurodegeneration. Although pathologically AD and CAA are well characterized diseases, the chronology of molecular changes that lead to their development is still unclear. Substantial evidence demonstrates defects in mitochondrial function in various cells of the neurovascular unit as well as in the brain parenchyma during the early stages of AD and CAA. Dysfunctional mitochondria release danger-associated molecular patterns (DAMPs) that activate a wide range of inflammatory pathways. In this review, we gather evidence to postulate a crucial role of the mitochondria, specifically of cerebral endothelial cells, as sensors and initiators of Aβ-induced vascular inflammation. The activated vasculature recruits circulating immune cells into the brain parenchyma, leading to the development of neuroinflammation and neurodegeneration in AD and CAA.

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Shahim, K., J. M. Drezet, J. F. Molinari, R. Sinkus, and S. Momjian. "Finite Element Analysis of Normal Pressure Hydrocephalus: Influence of CSF Content and Anisotropy in Permeability." Applied Bionics and Biomechanics 7, no. 3 (2010): 187–97. http://dx.doi.org/10.1155/2010/730658.

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Hydrocephalus is a cerebral disease where brain ventricles enlarge and compress the brain parenchyma towards the skull leading to symptoms like dementia, walking disorder and incontinence. The origin of normal pressure hydrocephalus is still obscure. In order to study this disease, a finite element model is built using the geometries of the ventricles and the skull measured by magnetic resonance imaging. The brain parenchyma is modelled as a porous medium fully saturated with cerebrospinal fluid (CSF) using Biot's theory of consolidation (1941). Owing to the existence of bundles of axons, the brain parenchyma shows locally anisotropic behaviour. Indeed, permeability is higher along the fibre tracts in the white matter region. In contrast, grey matter is isotropic. Diffusion tensor imaging is used to establish the local CSF content and the fibre tracts direction together with the associated local frame where the permeability coefficients are given by dedicated formulas. The present study shows that both inhomogeneous CSF content and anisotropy in permeability have a great influence on the CSF flow pattern through the parenchyma under an imposed pressure gradient between the ventricles and the subarachnoid spaces.

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Nwajei, Felix, Meenakshi Shanmugasundaram, Dana Paine, Anna Zal, Figen Beceren-Braun, Konrad Gabrisiewicz, Shouhao Zhou, et al. "Brain tumor-induced neuronal stress orchestrates adaptive immune surveillance through fractalkine." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 178.13. http://dx.doi.org/10.4049/jimmunol.200.supp.178.13.

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Abstract Tissue damage contributes to initiation and modulation of an immune response. Tumor progression generally causes distress to the surrounding tissue. However, how tumor-induced parenchymal damage regulates anti-tumor immune response remains to be understood. We found that tumors that invaded brain parenchyma compressed the surrounding neurons causing increased expression of the neuronal chemokine CX3CL1/fractalkine in the peritumoral margin. Intravital two-photon microscopy revealed perivascular recruitment of monocyte-derived CD11c+ dendritic cells and T cells that interacted and killed individual cancer cells in tumor margins. Immune surveillance of brain tumors became inefficient in mice lacking the receptor for fractalkine, CX3CR1, resulting in more aggressive tumor progression. Our results identify tissue stress and associated chemokine signaling as a potential target to orchestrate anti-tumor immune surveillance in the brain.

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Manning, H. Charles, Sheila D. Shay, and Robert A. Mericle. "Multispectral molecular imaging of capillary endothelium to facilitate preoperative endovascular brain mapping." Journal of Neurosurgery 110, no. 5 (May 2009): 975–80. http://dx.doi.org/10.3171/2008.9.jns08420.

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Object Brain mapping aims to localize neurological function to specific regions of the human brain. Preoperative endovascular brain mapping (PEBM) is a novel approach that allows clear visualization of nonfunctional (silent) brain parenchyma in real time during a resection. It has potential to improve neurosurgical guidance because brain shift does not alter the maps, and the map is visualized directly on the brain in situ rather than on a nearby image. Therefore, the risk of a new neurological deficit should be reduced. The authors report the first PEBM approach that combines selective molecular targeting of brain endothelium with multispectral (optical) imaging in preclinical animal models. Methods Sprague-Dawley rats and New Zealand white rabbits were selectively catheterized, and a fluorescein isothiocyanate–derivatized tomato lectin–based imaging probe was administered into the carotid artery or posterior cerebral artery, measuring < 500 μm in diameter. After binding/uptake of the imaging probe, and removal of unbound probe, a craniotomy was performed to directly visualize the “brain map.” Results Selective localization of the imaging probe to the right hemisphere in rats or right posterior cerebral artery in rabbits was clearly visualized after craniotomy. Cross-sections of stained capillaries demonstrated that the imaging probe did not cause vascular occlusion. Gross regional selectivity of the imaging probe was documented by multispectral molecular imaging of intact brains, with discrete localization and endothelium-directed targeting validated by histological examination. Conclusions The authors have demonstrated the first molecular endothelium-targeted approach to PEBM that does not require manipulation of the intact blood-brain barrier or result in vascular occlusion. Furthermore, the presented multispectral molecular imaging technique appears to be a suitable methodology for the generation of region-selective brain maps of vascularized brain parenchyma. Further refinement of the PEBM approach, as well as the development of improved imaging probes, may result in clinical advancement of PEBM where direct visual discrimination of nonfunctional silent brain parenchyma at the time of resection could significantly improve neurosurgical outcomes.

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Kleffman, Kevin, Grace Levinson, Indigo V. Rose, Lili Blumenberg, Sorin A. Shadaloey, Avantika Dhabaria, Eitan Wong, et al. "Abstract LB052: Melanoma-secreted amyloid beta suppresses neuroinflammation and promotes brain metastasis." Cancer Research 82, no. 12_Supplement (June 15, 2022): LB052. http://dx.doi.org/10.1158/1538-7445.am2022-lb052.

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Abstract Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate of brain metastasis among common cancer types, is an ideal model to study how cancer cells adapt to the brain parenchyma. Our unbiased proteomics analysis of melanoma short-term cultures revealed that proteins implicated in neurodegenerative pathologies are differentially expressed in melanoma cells explanted from brain metastases compared to those derived from extracranial metastases. We showed that melanoma cells require amyloid beta (Aβ) for growth and survival in the brain parenchyma. Melanoma-secreted Aβ activates surrounding astrocytes to a prometastatic, anti-inflammatory phenotype and prevents phagocytosis of melanoma by microglia. Finally, we demonstrate that pharmacological inhibition of Aβ decreases brain metastatic burden. Our results reveal a novel mechanistic connection between brain metastasis and Alzheimer’s disease - two previously unrelated pathologies, establish Aβ as a promising therapeutic target for brain metastasis, and demonstrate suppression of neuroinflammation as a critical feature of metastatic adaptation to the brain parenchyma. Citation Format: Kevin Kleffman, Grace Levinson, Indigo V. Rose, Lili Blumenberg, Sorin A. Shadaloey, Avantika Dhabaria, Eitan Wong, Francisco Galán-Echevarría, Alcida Karz, Diana Argibay, Richard Von-Itter, Alfredo Floristán, Gillian Baptiste, Nicole Eskow, James Tranos, Jenny Chen, Eleazar C. Vega Saenz de Miera, Melissa Call, Robert Rogers, George Jour, Youssef Zaim Wadghiri, Iman Osman, Yue Ming Li, Paul Mathews, Ronald Demattos, Beatrix Ueberheide, Kelly Ruggles, Shane A. Liddelow, Robert J. Schneider, Eva Hernando. Melanoma-secreted amyloid beta suppresses neuroinflammation and promotes brain metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB052.

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Journal articles on the topic 'Brain parenchyma'

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