121 results found
Zhang N, Parr CJC, Birch AM, et al., 2018, The amyloid precursor protein binds to beta-catenin and modulates its cellular distribution, NEUROSCIENCE LETTERS, Vol: 685, Pages: 190-195, ISSN: 0304-3940
Sastre M, Van Leuven F, Gentleman SM, 2018, TauBI or not TauBI: what was the question?, BRAIN, Vol: 141, Pages: 2536-2539, ISSN: 0006-8950
Edison P, Donat CK, Sastre M, 2018, In vivo Imaging of Glial Activation in Alzheimer's Disease, FRONTIERS IN NEUROLOGY, Vol: 9, ISSN: 1664-2295
Donat C, Mirzaei N, Tang S-P, et al., 2018, Imaging of Microglial Activation in Alzheimer's Disease by [11C]PBR28 PET, Biomarkers for Alzheimer's disease drug development, Editors: Perneczky, Publisher: Humana Press, Pages: 323-339
Goldfinger M, Tilley B, Mediratta S, et al., 2018, Boxing and the brain: disruption of the neurovascular unit in chronic traumatic encephalopathy, 119th Meeting of the British-Neuropathological-Society (BNS) / Epilepsy Neuropathology Symposium, Publisher: WILEY, Pages: 29-29, ISSN: 0305-1846
Donat CK, Mirzaei N, Tang S-P, et al., 2018, Imaging of Microglial Activation in Alzheimer's Disease by [11C]PBR28 PET., Methods Mol Biol, Vol: 1750, Pages: 323-339
Deficits in neuronal function and synaptic plasticity in Alzheimer's disease (AD) are believed to be linked to microglial activation. A hallmark of reactive microglia is the upregulation of mitochondrial translocator protein (TSPO) expression. Positron emission tomography (PET) is a nuclear imaging technique that measures the distribution of trace doses of radiolabeled compounds in the body over time. PET imaging using the 2nd generation TSPO tracer [11C]PBR28 provides an opportunity for accurate visualization and quantification of changes in microglial density in transgenic mouse models of Alzheimer's disease (AD). Here, we describe the methodology for the in vivo use of [11C]PBR28 in AD patients and the 5XFAD transgenic mouse model of AD and compare the results against healthy individuals and wild-type controls. To confirm the results, autoradiography with [3H]PBR28 and immunochemistry was carried out in the same mouse brains. Our data shows that [11C]PBR28 is suitable as a tool for in vivo monitoring of microglial activation and may be useful to assess treatment response in future studies.
Donat CK, Mirzaei N, Tang S-P, et al., 2018, Erratum to: Imaging of Microglial Activation in Alzheimer's Disease by [11C]PBR28 PET., Methods Mol Biol, Vol: 1750
Sidoryk-Wegrzynowicz M, Gerber YN, Ries M, et al., 2017, Astrocytes in mouse models of tauopathies acquire early deficits and lose neurosupportive functions, ACTA NEUROPATHOLOGICA COMMUNICATIONS, Vol: 5, ISSN: 2051-5960
Katsouri L, Lim YM, Eleftheriadou I, et al., 2016, PGC-1 alpha overexpression by lentiviral vector attenuates amyloid-beta load and neuronal loss in an Alzheimer's disease model, Conference on Changing the Face of Modern Medicine - Stem Cells and Gene Therapy, Publisher: MARY ANN LIEBERT, INC, Pages: A27-A27, ISSN: 1043-0342
Blondrath K, Steel JH, Katsouri L, et al., 2016, The nuclear cofactor receptor interacting protein-140 (RIP140) regulates the expression of genes involved in A beta generation, NEUROBIOLOGY OF AGING, Vol: 47, Pages: 180-191, ISSN: 0197-4580
Katsouri L, Lim YM, Blondrath K, et al., 2016, PPAR gamma-coactivator-1 alpha gene transfer reduces neuronal loss and amyloid-beta generation by reducing beta-secretase in an Alzheimer's disease model, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 113, Pages: 12292-12297, ISSN: 0027-8424
Ries M, Loiola R, Shah UN, et al., 2016, The anti-inflammatory Annexin A1 induces the clearance and degradation of the amyloid-beta peptide, JOURNAL OF NEUROINFLAMMATION, Vol: 13, ISSN: 1742-2094
Ries M, Sastre M, 2016, Mechanisms of A beta Clearance and Degradation by Glial Cells, FRONTIERS IN AGING NEUROSCIENCE, Vol: 8, ISSN: 1663-4365
Tang SP, Mirzaei N, Coello C, et al., 2016, EVALUATION OF [11C]PBR28 PET IMAGING TO DETECT CHANGES IN MICROGLIAL ACTIVATION IN MOUSE MODELS OF ALZHEIMER'S DISEASE, 27th International Symposium on Cerebral Blood Flow, Metabolism and Function / 12th International Conference on Quantification of Brain Function with PET, Publisher: SAGE PUBLICATIONS INC, Pages: 654-655, ISSN: 0271-678X
Mirzaei N, Sac PT, Ashworth S, et al., 2016, In Vivo Imaging of Microglial Activation by Positron Emission Tomography with [C-11] PBR28 in the 5XFAD Model of Alzheimer's Disease, GLIA, Vol: 64, Pages: 993-1006, ISSN: 0894-1491
Parr C, Carzaniga R, Gentleman SM, et al., 2016, Glycogen Synthase Kinase 3 Inhibition Promotes Lysosomal Biogenesis and Autophagic Degradation of the Amyloid-beta Precursor Protein (vol 32, pg 4410, 2012), MOLECULAR AND CELLULAR BIOLOGY, Vol: 36, Pages: 1219-1219, ISSN: 0270-7306
Mirzaei N, de Burgh R, Sharp D, et al., 2016, Evaluation of [3H]PBR28 as a marker of microglial activation in the rat controlled cortical impact model of traumatic brain injury, Publisher: TAYLOR & FRANCIS INC, Pages: 608-608, ISSN: 0269-9052
Birch AM, Cheung J, 2016, Alterations in the Expression of Transcription Factors PPARγ and NFκB in the Brain of Models of Chronic Pain, Biochemistry & Pharmacology: Open Access, Vol: 5
Sastre M, Ritchie CW, Hajji N, 2015, Metal Ions in Alzheimer’s disease brain, JSM Alzheimer’s Disease and Related Dementia, Vol: 2
There is substantial evidence supporting a critical role for metal ions in thepathogenesis of Alzheimer’s disease (AD). This originated with the observation thatcertain metal ions (principally copper, iron and zinc) are enriched in the neuriticplaques of AD brains, leading to an overall reduction in their bioavailability, suchas in the synaptic cleft. Imbalances of metal ions associated with aging and AD mayaffect the disease progression, leading to metals being reduced or increased fromtheir physiological steady state. Because metals ions are essential cofactors for manyproteins and they can compete with each other for binding to proteins, it is essentialto maintain metal homeostasis in order to preserve neuronal function. Some heavymetals may aggravate the progression of the disease due to their high neurotoxicityand their ability to induce epigenetic changes. On the other hand, alterations inthe levels of certain metal ions in other compartments in the brain could affect Aβenzymatic degradation, increase Aβ and tau aggregation as well as the processing ofthe amyloid precursor protein (APP) and other intracellular processes. Metal ions arealso instrumental in enhancing the production of reactive oxygen species in the brain,which could have consequences for neuronal viability and function. Here we review thestudies reporting the concentrations in brain, CSF and plasma in AD patients and howalterations in their transport and storage mechanisms can lead to their redistribution inthe brain, contributing to AD neuropathology.
Katsouri L, Ashraf A, Birch AM, et al., 2015, Systemic administration of fibroblast growth factor-2 (FGF2) reduces BACE1 expression and amyloid pathology in APP23 mice, NEUROBIOLOGY OF AGING, Vol: 36, Pages: 821-831, ISSN: 0197-4580
Parr C, Mirzaei N, Christian M, et al., 2015, Activation of the Wnt/beta-catenin pathway represses the transcription of the beta-amyloid precursor protein cleaving enzyme (BACE1) via binding of T-cell factor-4 to BACE1 promoter, FASEB JOURNAL, Vol: 29, Pages: 623-635, ISSN: 0892-6638
Mirzaei N, Parr C, Christian M, et al., 2014, Activation of the WNT/B-catenin pathway represses the transcription of the B-APP cleaving enzyme (BACE1), Publisher: Elsevier, ISSN: 1552-5279
Blondrath K, Sastre M, 2014, The ppargamma cofactor RIP140 regulates BACE1 gene expression, Publisher: Elsevier, ISSN: 1552-5279
Katsouri L, Lim YM, Mazarakis N, et al., 2014, PGC-1α GENE THERAPY IMPROVES MEMORY AND DECREASES AMYLOID BETA IN APP23 MICE, Pages: P256-P256, ISSN: 1552-5260
, 2014, Neuroinflammation in Alzheimer's, Parkinson's and Huntington's Diseases, Neuroinflammation and CNS Disorders, Pages: 111-150, ISBN: 9781118406557
© 2014 John Wiley & Sons, Ltd. All rights reserved. Neuroinflammation and oxidative stress are involved in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases. This is caused mainly by the presence of misfolded proteins which act as a catalyst for the activation and sustained activity of glial cells. Activated microglial cells are involved in both the initiation and progression of the disease, which will lead to the release of many pro-inflammatory mediators which induce neuronal injury and death. In addition, astrocytes may play an important role; their ability to secrete important neurotrophic factors may be impaired, while the release of pro-inflammatory cytokines may contribute to the cellular destruction. Activation of the innate and adaptive immune responses is evident in these diseases, while the production of reactive oxygen and nitrogen species will contribute to the neuronal destruction. This edition first published 2014
Torres M, Price SL, Fiol-deRoque MA, et al., 2014, Membrane lipid modifications and therapeutic effects mediated by hydroxydocosahexaenoic acid on Alzheimer's disease, BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES, Vol: 1838, Pages: 1680-1692, ISSN: 0005-2736
Birch AM, Katsouri L, Sastre M, 2014, Modulation of inflammation in transgenic models of Alzheimer's disease, JOURNAL OF NEUROINFLAMMATION, Vol: 11, ISSN: 1742-2094
Hajji N, Calvert C, Rtichie CW, et al., 2013, The role of metals in Alzheimer’s disease., Editors: Dexter D, Ward R, Crichton R, Dexter, Ward, Crichton, Publisher: The royal society of Chemistry (3 Jun 2013).
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.