نتائج البحث - "Monique Hooley"

المصدر: Jochems, A, Arteaga Reyes, C, Chappell, F M, Ritakari, T, Hooley, M, Doubal, F, Muñoz Maniega, S & Wardlaw, J M 2022, ' Longitudinal changes of white matter hyperintensities in sporadic small vessel disease: a systematic review and meta-analysis ', medrXiv . https://doi.org/10.1212/WNL.0000000000201205, https://doi.org/10.1101/2022.03.22.22272696

مصطلحات موضوعية: Adult, Stroke, Cerebral Small Vessel Diseases, Leukoaraiosis, Humans, Neurology (clinical), White Matter, Magnetic Resonance Imaging

وصف الملف: application/pdf

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5c170eafae40276ac3fb0b930ca84b69
https://doi.org/10.1212/wnl.0000000000201205

5

A role for astrocytes and microglia in synapse loss in Alzheimer’s disease

المؤلفون: Makis Tzioras, Michael Daniels, Caitlin Davies, Monique Hooley, Xin He, Owen R. Dando, Giles Hardingham, Barry McColl, Tara L. Spires‐Jones

المصدر: Alzheimer's & Dementia. 17

مصطلحات موضوعية: Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Neurology (clinical), Geriatrics and Gerontology

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::ca55c2434c22ddbd417bbca1125a5f47
https://doi.org/10.1002/alz.052532

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6

TMEM97 increases in synapses and is a potential synaptic Aβ binding partner in human Alzheimer’s disease

المؤلفون: Tara L. Spires-Jones, Monique Hooley, Colin Smith, Anton-Fernandez A, Jamie Rose, Susan M. Catalano, Makis Tzioras, Rosemary J. Jackson, J. H. Catterson, Nicholas J. Izzo, Claire L. Davies, Tempelaar R, Martí Colom-Cadena, Jane Tulloch, Sophie Dunnett

مصطلحات موضوعية: Synapse, Temporal cortex, Receptor complex, biology, Amyloid beta, Chemistry, Postsynaptic potential, Allosteric regulation, biology.protein, Cognitive decline, Postsynaptic density, Neuroscience

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::ed92cd0edcf16138aa25188d4a80a123
https://doi.org/10.1101/2021.02.01.428238

7

Residues W320 and Y328 within the binding site of the μ-opioid receptor influence opiate ligand bias

المؤلفون: Rubben Torella, Monique Hooley, J. Daniel Hothersall, Sarah A. Nickolls, Alastair J. H. Brown, Gordon McMurray, Sian Humphreys

المصدر: Neuropharmacology. 118:46-58

مصطلحات موضوعية: Models, Molecular, 0301 basic medicine, G-Protein-Coupled Receptor Kinase 2, medicine.drug_class, Stereochemistry, Narcotic Antagonists, Receptors, Opioid, mu, Diprenorphine, Transfection, Tritium, 03 medical and health sciences, chemistry.chemical_compound, Cellular and Molecular Neuroscience, Opioid receptor, Cyclic AMP, medicine, Humans, Binding site, Receptor, beta-Arrestins, G protein-coupled receptor, Pharmacology, Binding Sites, Chemistry, Tryptophan, Endomorphin-1, Enkephalin, Ala(2)-MePhe(4)-Gly(5), Ligand (biochemistry), Analgesics, Opioid, DAMGO, HEK293 Cells, 030104 developmental biology, Mutagenesis, Mutation, Biophysics, Tyrosine, Oligopeptides, Signal Transduction, medicine.drug

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0d3b0dcc0b296770be7b290c048ce1c6

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8

Reducing Tau Ameliorates Behavioural and Transcriptional Deficits in a Novel Model of Alzheimer's Disease

المصدر: SSRN Electronic Journal.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a1482a83efa2e99fe779eada6a1396b3
https://doi.org/10.2139/ssrn.3244529

9

Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer’s Disease

المصدر: Cell Reports
Cell Reports, Vol 29, Iss 11, Pp 3592-3604.e5 (2019)
Pickett, E K, Herrmann, A G, McQueen, J, Abt, K, Dando, O, Tulloch, J, Jain, P, Dunnett, S, Sohrabi, S, Fjeldstad, M P, Calkin, W, Murison, L, Jackson, R J, Tzioras, M, Stevenson, A, d'Orange, M, Hooley, M, Davies, C, Colom Cadena, M, Anton Fernandez, A, King, D, Oren, I, Rose, J, McKenzie, C-A, Allison, E, Smith, C, Hardt, O, Henstridge, C M, Hardingham, G E & Spires-Jones, T L 2019, ' Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer’s Disease ', Cell Reports, vol. 29, no. 11, pp. 3592-3604.E5 . https://doi.org/10.1016/j.celrep.2019.11.044

مصطلحات موضوعية: Male, 0301 basic medicine, Amyloid beta, Tau protein, Spatial Behavior, microglia, tau Proteins, Disease, Article, General Biochemistry, Genetics and Molecular Biology, Synapse, Mice, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Alzheimer Disease, synapse, Transcription (biology), mental disorders, medicine, Animals, Humans, tau, lcsh:QH301-705.5, array tomography, Aged, Aged, 80 and over, Amyloid beta-Peptides, biology, Microglia, Phenotype, amyloid beta, 030104 developmental biology, medicine.anatomical_structure, lcsh:Biology (General), Synapses, Alzheimer, biology.protein, Female, Transcriptome, Neuroscience, 030217 neurology & neurosurgery

وصف الملف: application/pdf

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b3ffb44a0caf216a757c3748b4edb3be

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