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Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease
by
Bradford, Barry M.
, Reynolds, Joe
, Verity, Nicholas
, Walmsley-Rowe, Lauryn
, Mabbott, Neil A.
in
631/378/2596/1308
/ 692/699/375/1937
/ Adhesion
/ Animals
/ Astrocyte
/ Astrocytes
/ Astrocytes - metabolism
/ Astrocytes - pathology
/ Brain - metabolism
/ Brain - pathology
/ CD44 antigen
/ Cell adhesion molecule CD44
/ Cell adhesion molecules
/ Cell surface
/ Dendritic plasticity
/ Dendritic spines
/ Disease
/ Humanities and Social Sciences
/ Hyaluronan Receptors - genetics
/ Hyaluronan Receptors - metabolism
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ Microglia
/ Microglia - metabolism
/ Microglia - pathology
/ multidisciplinary
/ Neurodegeneration
/ Neurodegenerative diseases
/ Neuropathogenesis
/ Prion disease
/ Prion Diseases - genetics
/ Prion Diseases - metabolism
/ Prion Diseases - pathology
/ Prion protein
/ Protein folding
/ Science
/ Science (multidisciplinary)
/ Spine
/ Synapses
/ Synaptic plasticity
2024
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Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease
by
Bradford, Barry M.
, Reynolds, Joe
, Verity, Nicholas
, Walmsley-Rowe, Lauryn
, Mabbott, Neil A.
in
631/378/2596/1308
/ 692/699/375/1937
/ Adhesion
/ Animals
/ Astrocyte
/ Astrocytes
/ Astrocytes - metabolism
/ Astrocytes - pathology
/ Brain - metabolism
/ Brain - pathology
/ CD44 antigen
/ Cell adhesion molecule CD44
/ Cell adhesion molecules
/ Cell surface
/ Dendritic plasticity
/ Dendritic spines
/ Disease
/ Humanities and Social Sciences
/ Hyaluronan Receptors - genetics
/ Hyaluronan Receptors - metabolism
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ Microglia
/ Microglia - metabolism
/ Microglia - pathology
/ multidisciplinary
/ Neurodegeneration
/ Neurodegenerative diseases
/ Neuropathogenesis
/ Prion disease
/ Prion Diseases - genetics
/ Prion Diseases - metabolism
/ Prion Diseases - pathology
/ Prion protein
/ Protein folding
/ Science
/ Science (multidisciplinary)
/ Spine
/ Synapses
/ Synaptic plasticity
2024
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Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease
by
Bradford, Barry M.
, Reynolds, Joe
, Verity, Nicholas
, Walmsley-Rowe, Lauryn
, Mabbott, Neil A.
in
631/378/2596/1308
/ 692/699/375/1937
/ Adhesion
/ Animals
/ Astrocyte
/ Astrocytes
/ Astrocytes - metabolism
/ Astrocytes - pathology
/ Brain - metabolism
/ Brain - pathology
/ CD44 antigen
/ Cell adhesion molecule CD44
/ Cell adhesion molecules
/ Cell surface
/ Dendritic plasticity
/ Dendritic spines
/ Disease
/ Humanities and Social Sciences
/ Hyaluronan Receptors - genetics
/ Hyaluronan Receptors - metabolism
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ Microglia
/ Microglia - metabolism
/ Microglia - pathology
/ multidisciplinary
/ Neurodegeneration
/ Neurodegenerative diseases
/ Neuropathogenesis
/ Prion disease
/ Prion Diseases - genetics
/ Prion Diseases - metabolism
/ Prion Diseases - pathology
/ Prion protein
/ Protein folding
/ Science
/ Science (multidisciplinary)
/ Spine
/ Synapses
/ Synaptic plasticity
2024
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Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease
Journal Article
Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease
2024
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Overview
Prion diseases are fatal, infectious, neurodegenerative disorders resulting from accumulation of misfolded cellular prion protein in the brain. Early pathological changes during CNS prion disease also include reactive astrocyte activation with increased CD44 expression, microgliosis, as well as loss of dendritic spines and synapses. CD44 is a multifunctional cell surface adhesion and signalling molecule which is considered to play roles in astrocyte morphology and the maintenance of dendritic spine integrity and synaptic plasticity. However, the role of CD44 in prion disease was unknown. Here we used mice deficient in CD44 to determine the role of CD44 during prion disease. We show that CD44-deficient mice displayed no difference in their response to CNS prion infection when compared to wild type mice. Furthermore, the reactive astrocyte activation and microgliosis that accompanies CNS prion infection was unimpaired in the absence of CD44. Together, our data show that although CD44 expression is upregulated in reactive astrocytes during CNS prion disease, it is dispensable for astrocyte and microglial activation and the development of prion neuropathogenesis.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
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