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AAIC 2022 | Reactive astrocytes show opposing functions in Alzheimer’s disease and Huntington’s disease

Carole Escartin, PhD, Centre National de la Recherche Scientifique, Université Paris Saclay, Fontenay-aux-roses, France, describes her research into the molecular and functional changes in reactive astrocytes and the signaling cascades that control them in vivo. Recent findings have shown that the role astrocytes play is highly context-dependent, showing variability between diseases and across disease course. For example, work from the Escartin lab to block astrocyte reactivity through viral vector targeting of the JAK-STAT3 pathway showed improvement in mouse models of Alzheimer’s disease: reduced amyloid deposition, improved learning, and restored synaptic plasticity. Whereas the opposite effect was seen in animal models of Huntington’s disease. Newly published data showed that selective activation of the JAK-STAT3 cascade through viral gene transfer reduced mutant Huntingtin aggregation, improved neuronal deficits, reduced striatal atrophy, and increased glutamate levels. Those opposing findings demonstrate the complex nature of astrocyte activity in health and disease. How the reactive state is controlled and what functional impacts these changes have needs to be investigated in more detail in order to fine tune astrocyte manipulation and identify new targets to promote their neuroprotective functions. This interview took place at the Alzheimer’s Association International Conference (AAIC) 2022 in San Diego, CA.