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Jiwaji, Zoeb; Tiwari, Sachin S; Avilés-Reyes, Rolando X; Hooley, Monique; Hampton, David; Torvell, Megan; Johnson, Delinda A; McQueen, Jamie; Baxter, Paul; Sabari-Sankar, Kayalvizhi; Qiu, Jing; He, Xin; Fowler, Jill; Febery, James; Gregory, Jenna; Rose, Jamie; Tulloch, Jane; Loan, Jamie; Story, David; McDade, Karina; Smith, Amy M; Greer, Peta; Ball, Matthew; Kind, Peter C; Matthews, Paul M; Smith, Colin; Dando, Owen; Spires-Jones, Tara L; Johnson, Jeffrey A; Chandran, Siddharthan; Hardingham, Giles E
Nature communications, 01/2022, Volume: 13, Issue: 1Journal Article
Alzheimer's disease (AD) alters astrocytes, but the effect of Aß and Tau pathology is poorly understood. TRAP-seq translatome analysis of astrocytes in APP/PS1 ß-amyloidopathy and MAPT tauopathy mice revealed that only Aß influenced expression of AD risk genes, but both pathologies precociously induced age-dependent changes, and had distinct but overlapping signatures found in human post-mortem AD astrocytes. Both Aß and Tau pathology induced an astrocyte signature involving repression of bioenergetic and translation machinery, and induction of inflammation pathways plus protein degradation/proteostasis genes, the latter enriched in targets of inflammatory mediator Spi1 and stress-activated cytoprotective Nrf2. Astrocyte-specific Nrf2 expression induced a reactive phenotype which recapitulated elements of this proteostasis signature, reduced Aß deposition and phospho-tau accumulation in their respective models, and rescued brain-wide transcriptional deregulation, cellular pathology, neurodegeneration and behavioural/cognitive deficits. Thus, Aß and Tau induce overlapping astrocyte profiles associated with both deleterious and adaptive-protective signals, the latter of which can slow patho-progression.
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