Post-mortem studies in patients with Alzheimer’s disease (AD) suggest that amyloid-β (Aβ) and tau pathologies are associated with astrocyte reactivity. Transcriptomics analyses have also demonstrated that reactive astrocytes are able to adopt different molecular phenotypes in the brain. João Pedro Ferrari-Souza, MD-PhD student, University of Pittsburgh, Pittsburgh, explains his research into Aβ- and tau-specific contributions to levels of the reactive astrocyte biomarkers, glial fibrillary acidic protein (GFAP) and chitinase-3-like protein 1 (YKL-40). It was found that GFAP and YKL-40 were specifically associated with Aβ and tau pathology, respectively. Higher levels of GFAP in the cerebrospinal fluid (CSF) were associated with elevated tau-PET, but not Aβ-PET, while the reverse was found for CSF YKL-40 levels. These data indicate that reactive astrogliosis should not be defined based on one biomarker, as distinct astrocyte biomarker signatures may exist. This interview took place at the Clinical Trials on Alzheimer’s Disease congress 2022 in San Francisco.
These works are owned by Magdalen Medical Publishing (MMP) and are protected by copyright laws and treaties around the world. All rights are reserved.