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391 results on '"Jacobs, Russell E."'

1. Retraction Note: Pericyte degeneration causes white matter dysfunction in the mouse central nervous system

Author

Montagne, Axel, Nikolakopoulou, Angeliki M., Zhao, Zhen, Sagare, Abhay P., Si, Gabriel, Lazic, Divna, Barnes, Samuel R., Daianu, Madelaine, Ramanathan, Anita, Go, Ariel, Lawson, Erica J., Wang, Yaoming, Mack, William J., Thompson, Paul M., Schneider, Julie A., Varkey, Jobin, Langen, Ralf, Mullins, Eric, Jacobs, Russell E., and Zlokovic, Berislav V.

Published
2024
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4. Vascular dysfunction-The disregarded partner of Alzheimer's disease.

Author

Sweeney, Melanie D, Montagne, Axel, Sagare, Abhay P, Nation, Daniel A, Schneider, Lon S, Chui, Helena C, Harrington, Michael G, Pa, Judy, Law, Meng, Wang, Danny JJ, Jacobs, Russell E, Doubal, Fergus N, Ramirez, Joel, Black, Sandra E, Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M, Markus, Hugh S, Salman, Rustam A, Allan, Stuart M, Quinn, Terence J, Kalaria, Rajesh N, Werring, David J, Carare, Roxana O, Touyz, Rhian M, Williams, Steve CR, Moskowitz, Michael A, Katusic, Zvonimir S, Lutz, Sarah E, Lazarov, Orly, Minshall, Richard D, Rehman, Jalees, Davis, Thomas P, Wellington, Cheryl L, González, Hector M, Yuan, Chun, Lockhart, Samuel N, Hughes, Timothy M, Chen, Christopher LH, Sachdev, Perminder, O'Brien, John T, Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R, Biessels, Geert Jan, Wallin, Anders, Smith, Eric E, Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique MB, Román, Gustavo C, Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F, van Buchem, Mark A, Arvanitakis, Zoe, Schneider, Julie A, Drewes, Lester R, Hachinski, Vladimir, Finch, Caleb E, Toga, Arthur W, Wardlaw, Joanna M, and Zlokovic, Berislav V

Subjects
Blood-Brain Barrier, Brain, Humans, Alzheimer Disease, Vascular Diseases, Cerebrovascular Circulation, United States, National Institute on Aging (U.S.), Amyloid beta-Peptides, White Matter, Biomarkers, Alzheimer's disease, Blood-brain barrier, Cerebral blood flow, MRI, Vascular, National Institute on Aging, Neurosciences, Clinical Sciences, Geriatrics
Abstract

Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging-Alzheimer's Association describes a biomarker-based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated with, and/or contributing to, AD pathophysiology, including changes in blood-brain barrier integrity and cerebral blood flow. Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize. We suggest that these vascular biomarkers should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.

Published
2019

8. Conditional Creation and Rescue of Nipbl-Deficiency in Mice Reveals Multiple Determinants of Risk for Congenital Heart Defects.

Author

Santos, Rosaysela, Kawauchi, Shimako, Jacobs, Russell E, Lopez-Burks, Martha E, Choi, Hojae, Wikenheiser, Jamie, Hallgrimsson, Benedikt, Jamniczky, Heather A, Fraser, Scott E, Lander, Arthur D, and Calof, Anne L

Subjects
Heart, Cell Line, Animals, Mice, Transgenic, Heart Septal Defects, Atrial, Genetic Predisposition to Disease, Transcription Factors, Risk Factors, Organ Specificity, Gene Expression, Penetrance, Female, Male, Genetic Association Studies, Haploinsufficiency, Homeobox Protein Nkx-2.5, Mice, Transgenic, Heart Septal Defects, Atrial, Pediatric, Heart Disease, Cardiovascular, Congenital Structural Anomalies, Rare Diseases, Genetics, Stem Cell Research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic Health Relevance, Developmental Biology, Biological Sciences, Medical and Health Sciences, Agricultural and Veterinary Sciences
Abstract

Elucidating the causes of congenital heart defects is made difficult by the complex morphogenesis of the mammalian heart, which takes place early in development, involves contributions from multiple germ layers, and is controlled by many genes. Here, we use a conditional/invertible genetic strategy to identify the cell lineage(s) responsible for the development of heart defects in a Nipbl-deficient mouse model of Cornelia de Lange Syndrome, in which global yet subtle transcriptional dysregulation leads to development of atrial septal defects (ASDs) at high frequency. Using an approach that allows for recombinase-mediated creation or rescue of Nipbl deficiency in different lineages, we uncover complex interactions between the cardiac mesoderm, endoderm, and the rest of the embryo, whereby the risk conferred by genetic abnormality in any one lineage is modified, in a surprisingly non-additive way, by the status of others. We argue that these results are best understood in the context of a model in which the risk of heart defects is associated with the adequacy of early progenitor cell populations relative to the sizes of the structures they must eventually form.

Published
2016

9. Synthesis and Preclinical Evaluation of 22-[18F]Fluorodocosahexaenoic Acid as a Positron Emission Tomography Probe for Monitoring Brain Docosahexaenoic Acid Uptake Kinetics

Author

Duro, Marlon Vincent V., primary, Van Valkenburgh, Juno, additional, Ingles, Diana E., additional, Tran, Jenny, additional, Cai, Zhiheng, additional, Ebright, Brandon, additional, Wang, Shaowei, additional, Kerman, Bilal E., additional, Galvan, Jasmin, additional, Hwang, Sung Hee, additional, Sta Maria, Naomi S., additional, Zanderigo, Francesca, additional, Croteau, Etienne, additional, Cunnane, Stephen C., additional, Rapoport, Stanley I., additional, Louie, Stan G., additional, Jacobs, Russell E., additional, Yassine, Hussein N., additional, and Chen, Kai, additional

Published
2023
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10. Manipulation of Dietary DHA does not Alter DHA Brain Uptake Kinetics in Mice Despite Changing Brain and Plasma DHA Levelsvs

Author

Duro, Marlon Vincent V., primary, Van Valkenburgh, Juno S., additional, Abdullah, Laila, additional, Ingles, Diana E., additional, Cai, Zhiheng, additional, Kerman, Bilal Ersen, additional, Wang, Shaowei, additional, Jacobs, Russell E., additional, Sta. Maria, Naomi, additional, Zanderigo, Francesca, additional, Croteau, Etienne, additional, Cunnane, Stephen, additional, Rapoport, Stanley I., additional, Chen, Kai, additional, and Yassine, Hussein N., additional

Published
2023
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13. Vascular dysfunction—The disregarded partner of Alzheimer's disease

Author

Sweeney, Melanie D., Montagne, Axel, Sagare, Abhay P., Nation, Daniel A., Schneider, Lon S., Chui, Helena C., Harrington, Michael G., Pa, Judy, Law, Meng, Wang, Danny J.J., Jacobs, Russell E., Doubal, Fergus N., Ramirez, Joel, Black, Sandra E., Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M., Markus, Hugh S., Salman, Rustam A., Allan, Stuart M., Quinn, Terence J., Kalaria, Rajesh N., Werring, David J., Carare, Roxana O., Touyz, Rhian M., Williams, Steve C.R., Moskowitz, Michael A., Katusic, Zvonimir S., Lutz, Sarah E., Lazarov, Orly, Minshall, Richard D., Rehman, Jalees, Davis, Thomas P., Wellington, Cheryl L., González, Hector M., Yuan, Chun, Lockhart, Samuel N., Hughes, Timothy M., Chen, Christopher L.H., Sachdev, Perminder, O'Brien, John T., Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R., Biessels, Geert Jan, Wallin, Anders, Smith, Eric E., Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique M.B., Román, Gustavo C., Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F., van Buchem, Mark A., Arvanitakis, Zoe, Schneider, Julie A., Drewes, Lester R., Hachinski, Vladimir, Finch, Caleb E., Toga, Arthur W., Wardlaw, Joanna M., and Zlokovic, Berislav V.

Published
2019
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15. Multimodality PET/MRI agents targeted to activated macrophages

Author

Tu, Chuqiao, Ng, Thomas SC, Jacobs, Russell E, and Louie, Angelique Y

Subjects
Inorganic Chemistry, Biochemistry and Cell Biology, Chemical Sciences, Biological Sciences, Biomedical Imaging, Nanotechnology, Bioengineering, Animals, Cell Line, Copper Radioisotopes, Dextrans, Ferric Compounds, Macrophage Activation, Macrophages, Magnetic Resonance Imaging, Nanoparticles, Particle Size, Positron-Emission Tomography, Rats, Surface Properties, Iron, MRI contrast agents, Inflammation, Medicinal and Biomolecular Chemistry, Biophysics, Biochemistry and cell biology, Inorganic chemistry
Abstract

The recent emergence of multimodality imaging, particularly the combination of PET and MRI, has led to excitement over the prospect of improving detection of disease. Iron oxide nanoparticles have become a popular platform for the fabrication of PET/MRI probes owing to their advantages of high MRI detection sensitivity, biocompatibility, and biodegradability. In this article, we report the synthesis of dextran-coated iron oxide nanoparticles (DIO) labeled with the positron emitter (64)Cu to generate a PET/MRI probe, and modified with maleic anhydride to increase the negative surface charge. The modified nanoparticulate PET/MRI probe (MDIO-(64)Cu-DOTA) bears repetitive anionic charges on the surface that facilitate recognition by scavenger receptor type A (SR-A), a ligand receptor found on activated macrophages but not on normal vessel walls. MDIO-(64)Cu-DOTA has an average iron oxide core size of 7-8 nm, an average hydrodynamic diameter of 62.7 nm, an r1 relaxivity of 16.8 mM(-1) s(-1), and an r 2 relaxivity of 83.9 mM(-1) s(-1) (37 °C, 1.4 T). Cell studies confirmed that the probe was nontoxic and was specifically taken up by macrophages via SR-A. In comparison with the nonmodified analog, the accumulation of MDIO in macrophages was substantially improved. These characteristics demonstrate the promise of MDIO-(64)Cu-DOTA for identification of vulnerable atherosclerotic plaques via the targeting of macrophages.

Published
2014

18. Comparison of Biomarkers in Transgenic Alzheimer Rats Using Multi-Shell Diffusion MRI

Author

Fick, Rutger H. J., Daianu, Madelaine, Pizzolato, Marco, Wassermann, Demian, Jacobs, Russell E., Thompson, Paul M., Town, Terrence, Deriche, Rachid, Hege, Hans-Christian, Series editor, Hoffman, David, Series editor, Polthier, Konrad, Series editor, Rumpf, Martin, Series editor, Fuster, Andrea, editor, Ghosh, Aurobrata, editor, Kaden, Enrico, editor, Rathi, Yogesh, editor, and Reisert, Marco, editor

Published
2017
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20. Synthesis and Preclinical Evaluation of 22‑[18F]Fluorodocosahexaenoic Acid as a Positron Emission Tomography Probe for Monitoring Brain Docosahexaenoic Acid Uptake Kinetics.

Author

Duro, Marlon Vincent V., Van Valkenburgh, Juno, Ingles, Diana E., Tran, Jenny, Cai, Zhiheng, Ebright, Brandon, Wang, Shaowei, Kerman, Bilal E., Galvan, Jasmin, Hwang, Sung Hee, Sta Maria, Naomi S., Zanderigo, Francesca, Croteau, Etienne, Cunnane, Stephen C., Rapoport, Stanley I., Louie, Stan G., Jacobs, Russell E., Yassine, Hussein N., and Chen, Kai

Published
2023
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21. Author Correction: APOE4 accelerates advanced-stage vascular and neurodegenerative disorder in old Alzheimer’s mice via cyclophilin A independently of amyloid-β

Author

Montagne, Axel, Nikolakopoulou, Angeliki M., Huuskonen, Mikko T., Sagare, Abhay P., Lawson, Erica J., Lazic, Divna, Rege, Sanket V., Grond, Alexandra, Zuniga, Edward, Barnes, Samuel R., Prince, Jacob, Sagare, Meghana, Hsu, Ching-Ju, LaDu, Mary J., Jacobs, Russell E., and Zlokovic, Berislav V.

Published
2021
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22. Pericyte degeneration causes white matter dysfunction in the mouse central nervous system

Author

Montagne, Axel, Nikolakopoulou, Angeliki M, Zhao, Zhen, Sagare, Abhay P, Si, Gabriel, Lazic, Divna, Barnes, Samuel R, Daianu, Madelaine, Ramanathan, Anita, Go, Ariel, Lawson, Erica J, Wang, Yaoming, Mack, William J, Thompson, Paul M, Schneider, Julie A, Varkey, Jobin, Langen, Ralf, Mullins, Eric, Jacobs, Russell E, and Zlokovic, Berislav V

Subjects
Neural circuitry -- Health aspects, Fibrin -- Health aspects, Central nervous system diseases -- Development and progression -- Care and treatment, Biological sciences, Health
Abstract

Diffuse white-matter disease associated with small-vessel disease and dementia is prevalent in the elderly. The biological mechanisms, however, remain elusive. Using pericyte-deficient mice, magnetic resonance imaging, viral-based tract-tracing, and behavior and tissue analysis, we found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons and oligodendrocytes. This disrupted brain circuits, leading to white-matter functional deficits before neuronal loss occurs. Fibrinogen and fibrin fibrils initiated autophagy-dependent cell death in oligodendrocyte and pericyte cultures, whereas pharmacological and genetic manipulations of systemic fibrinogen levels in pericyte-deficient, but not control mice, influenced the degree of white-matter fibrin(ogen) deposition, pericyte degeneration, vascular pathology and white-matter changes. Thus, our data indicate that pericytes control white-matter structure and function, which has implications for the pathogenesis and treatment of human white-matter disease associated with small-vessel disease., Author(s): Axel Montagne [1, 2]; Angeliki M Nikolakopoulou [1, 2]; Zhen Zhao [1, 2]; Abhay P Sagare [1, 2]; Gabriel Si [1]; Divna Lazic [1, 2, 3]; Samuel R Barnes [...]

Published
2018
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23. RETRACTED ARTICLE: Pericyte degeneration causes white matter dysfunction in the mouse central nervous system

Author

Montagne, Axel, Nikolakopoulou, Angeliki M, Zhao, Zhen, Sagare, Abhay P, Si, Gabriel, Lazic, Divna, Barnes, Samuel R, Daianu, Madelaine, Ramanathan, Anita, Go, Ariel, Lawson, Erica J, Wang, Yaoming, Mack, William J, Thompson, Paul M, Schneider, Julie A, Varkey, Jobin, Langen, Ralf, Mullins, Eric, Jacobs, Russell E, and Zlokovic, Berislav V

Published
2018
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40. Early Life Adversity Potentiates Adult Response to Acute Threat: A Brain-wide Neuroimaging and Behavior Study

Author

Uselman, Taylor W., Jacobs, Russell E., and Bearer, Elaine L.

Abstract

Adverse childhood experiences increase vulnerability to stress-provoked mental illnesses, such as anxiety/depression and substance use disorders, later in life. How these experiences shape the brain to lead to such disorders remains a mystery. Brain-wide imaging of neural activity in the adult raised with or without early life adversity (ELA) holds promise of finding clues. Longitudinal manganese-enhanced magnetic resonance imaging (MEMRI) provides a methodology to follow brain-wide neural activity dynamics over time in awake-behaving animals. Mn(II) delivered systemically is taken up through voltage-gated calcium channels throughout the brain over 24-26h. Behavior is recorded in our custom arena during Mn(II) uptake. We capture an image of basal behavior (normal exploration) at 22h, and then expose mice to acute threat, predator odor (TMT, 2,3,5-Trimethyl-3-thiazoine), and image again at 26h (Uselman et al, 2020). Here we combine this MEMRI paired with behavior protocol to investigate the effects of ELA on responses to acute threat in normally reared (n=12) and maternally deprived mice (n=12) (ELA-/+). Dams with newborn pups were deprived of adequate bedding from day P2-P9, which induces elevated cortisol in the pups (Rice et al., 2008). At 10 weeks of age, mice +/- ELA were subject our paired behavior-MEMRI longitudinal procedure for both acute and delayed responses. After imaging, mice are sacrificed, brains perfusion fixed and serial sections stained by immunohistochemistry. MEMRI images were skull-stripped, spatially co-registered, and intensity normalized. To measure the degree of activity and relationships between brain regions we performed statistical parametric mapping (SPM), segmentation of 90 brain regions, cross-correlation analysis, and Louvain community detection. Predator stress increased defensive/avoidance behavior for both groups (p

Published
2021

50. Prenatal disruption of blood-brain barrier formation via cyclooxygenase activation leads to lifelong brain inflammation.

Author

Qiuying Zhao, Weiye Dai, Hui Yu Chen, Jacobs, Russell E., Zlokovic, Berislav V., Lund, Brett T., Montagne, Axel, and Bonnin, Alexandre

Subjects
BLOOD-brain barrier, ENCEPHALITIS, MATERNAL immune activation, MYELOID cells, NEUROBEHAVIORAL disorders, COMMERCIAL products, CURCUMIN
Abstract

Gestational maternal immune activation (MIA) in mice induces persistent brain microglial activation and a range of neuropathologies in the adult offspring. Although longterm phenotypes are well documented, how MIA in utero leads to persistent brain inflammation is not well understood. Here, we found that offspring of mothers treated with polyriboinosinic-polyribocytidylic acid [poly(I:C)] to induce MIA at gestational day 13 exhibit blood-brain barrier (BBB) dysfunction throughout life. Live MRI in utero revealed fetal BBB hyperpermeability 2 d after MIA. Decreased pericyte-endothelium coupling in cerebral blood vessels and increased microglial activation were found in fetal and 1- and 6-mo-old offspring brains. The long-lasting disruptions result from abnormal prenatal BBB formation, driven by increased proliferation of cyclooxygenase-2 (COX2; Ptgs2)-expressing microglia in fetal brain parenchyma and perivascular spaces. Targeted deletion of the Ptgs2 gene in fetal myeloid cells or treatment with the inhibitor celecoxib 24 h after immune activation prevented microglial proliferation and disruption of BBB formation and function, showing that prenatal COX2 activation is a causal pathway of MIA effects. Thus, gestational MIA disrupts fetal BBB formation, inducing persistent BBB dysfunction, which promotes microglial overactivation and behavioral alterations across the offspring life span. Taken together, the data suggest that gestational MIA disruption of BBB formation could be an etiological contributor to neuropsychiatric disorders. [ABSTRACT FROM AUTHOR]

Published
2022
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