Bruna Bellaver, PhD, University of Pittsburgh, Pittsburgh, PA, describes an investigation into astrocyte reactivity and its impact on subsequent tau pathology development. This study was conducted in cognitively unimpaired (CU) individuals, looking at plasma p-tau and plasma GFAP as an indicator of astrocyte reactivity. It was observed that amyloid-β (Aβ) was only associated with increased plasma p-tau levels in individuals with astrocyte reactivity. Cross-sectional and longitudinal PET analyses also showed that tau only accumulated in response to Aβ in those with astrocyte reactivity. This is a step in understanding why some people with Aβ pathology do not develop Alzheimer’s disease (AD) symptoms. Mechanistically, it is suggested that the Aβ is triggering these astrocytes and the subsequent release of mediators, which trigger tau pathology accumulation. For the future, the team are looking to answer why Aβ triggers astrocytes in some cases but not others. This interview took place at the AD/PD™ 2023 congress in Gothenburg, Sweden.
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