Post by Nadica (She/Her) on Jul 25, 2024 2:53:31 GMT
Temporal progression of tau pathology and neuroinflammation in a rhesus monkey model of Alzheimer’s disease - Published April 8, 2024\
Posting this article as the study of neuroinflammation is critical to understanding covid and long covid: We may be seeing this study quoted in the future
Abstract
INTRODUCTION: The understanding of the pathological events in Alzheimer’s disease (AD) has advanced dramatically, but the successful translation from rodent models into efficient human therapies is still problematic.
METHODS: To examine how tau pathology can develop in the primate brain, we injected 12 macaques with a dual tau mutation (P301L/S320F) into the entorhinal cortex (ERC). An investigation was performed using high-resolution microscopy, magnetic resonance imaging (MRI), positron emission tomography (PET), and fluid biomarkers to determine the temporal progression of the pathology 3 and 6 months after the injection.
RESULTS: Using quantitative microscopy targeting markers for neurodegeneration and neuroinflammation, as well as fluid and imaging biomarkers, we detailed the progression of misfolded tau spreading and the consequential inflammatory response induced by glial cells.
DISCUSSION: By combining the analysis of several in vivo biomarkers with extensive brain microscopy analysis, we described the initial steps of misfolded tau spreading and neuroinflammation in a monkey model highly translatable to AD patients
Posting this article as the study of neuroinflammation is critical to understanding covid and long covid: We may be seeing this study quoted in the future
Abstract
INTRODUCTION: The understanding of the pathological events in Alzheimer’s disease (AD) has advanced dramatically, but the successful translation from rodent models into efficient human therapies is still problematic.
METHODS: To examine how tau pathology can develop in the primate brain, we injected 12 macaques with a dual tau mutation (P301L/S320F) into the entorhinal cortex (ERC). An investigation was performed using high-resolution microscopy, magnetic resonance imaging (MRI), positron emission tomography (PET), and fluid biomarkers to determine the temporal progression of the pathology 3 and 6 months after the injection.
RESULTS: Using quantitative microscopy targeting markers for neurodegeneration and neuroinflammation, as well as fluid and imaging biomarkers, we detailed the progression of misfolded tau spreading and the consequential inflammatory response induced by glial cells.
DISCUSSION: By combining the analysis of several in vivo biomarkers with extensive brain microscopy analysis, we described the initial steps of misfolded tau spreading and neuroinflammation in a monkey model highly translatable to AD patients