Overexpression of pathogenic tau in astrocytes causes a reduction in AQP4 and GLT1, an immunosuppressed phenotype and unique transcriptional responses to repetitive mild TBI without appreciable changes in tauopathy.

Document Type

Article

Abstract

Epidemiological studies have unveiled a robust link between exposure to repetitive mild traumatic brain injury (r-mTBI) and elevated susceptibility to develop neurodegenerative disorders, notably chronic traumatic encephalopathy (CTE). The pathogenic lesion in CTE cases is characterized by the accumulation of hyperphosphorylated tau in neurons around small cerebral blood vessels which can be accompanied by astrocytes that contain phosphorylated tau, the latter termed tau astrogliopathy. However, the contribution of tau astrogliopathy to the pathobiology and functional consequences of r-mTBI/CTE or whether it is merely a consequence of aging remains unclear. We addressed these pivotal questions by utilizing a mouse model harboring tau-bearing astrocytes, GFAP

Keywords

Animals, Humans, Male, Mice, Aquaporin 4, Astrocytes, Brain Concussion, Excitatory Amino Acid Transporter 2, Mice, Inbred C57BL, Mice, Transgenic, Phenotype, tau Proteins, Tauopathies

Medical Subject Headings

Animals; Humans; Male; Mice; Aquaporin 4; Astrocytes; Brain Concussion; Excitatory Amino Acid Transporter 2; Mice, Inbred C57BL; Mice, Transgenic; Phenotype; tau Proteins; Tauopathies

Publication Date

5-15-2024

Publication Title

Journal of neuroinflammation [electronic resource]

ISSN

1742-2094

Volume

21

Issue

1

First Page

130

Last Page

130

PubMed ID

38750510

Digital Object Identifier (DOI)

10.1186/s12974-024-03117-4

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