Amyloid-beta and tau pathologies are both necessary to induce novel stage-specific microglia subtypes during Alzheimer's disease progression.
Kim, D. W.; Tu, K.; Wei, A.; Lau, A.; Gonzalez-Gil, A.; Cao, T.; Braunstein, K.; Ling, J. P.; Troncoso, J. C.; Wong, P. C.; Blackshaw, S.; Schnaar, R. L.; Li, T.
Show abstract
It is unknown whether specific microglia are selectively induced by amyloid-{beta} (A{beta}), tau pathologies, or both in combination. To address this, we use single-cell RNA-sequencing to profile mice bearing both A{beta} and tau pathologies during Alzheimers disease (AD) progression. We identify novel microglia subtypes induced in a disease stage-specific manner. We show that during early-stage disease, interferon signaling induces a subtype of microglia termed EADAM. During late-stage disease, a second microglia subtype termed LADAM is detected. While EADAM and LADAM-like microglia are observed in other neurodegenerative models, the magnitude and composition of subtype markers are distinct from microglia observed with AD-like pathology. The pattern of EADAM- and LADAM-associated gene expression is observed in microglia from human AD, during the early and late stages of disease, respectively. Furthermore, we observe that several siglec genes are selectively expressed in either EADAM or LADAM. Siglecg is expressed in white-matter-associated LADAM, and expression of the human orthologue of Siglecg is progressively elevated in AD-stage-dependent manner but not shown in non-AD tauopathy. Our findings imply that both A{beta} and tau pathologies are required for disease stage-specific induction of EADAM and LADAM.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- A public resource of single cell transcriptomes and multiscale networks from persons with and without Alzheimer's disease 98%
- Novel brain-penetrant inhibitor of G9a methylase blocks Alzheimer’s disease proteopathology for precision medication 97%
- Cell-type-specific Alzheimer’s disease polygenic risk scores are associated with distinct disease processes in Alzheimer’s disease 97%
Similar papers in this journal
- Sustained TREM2 stabilization accelerates microglia heterogeneity and Abeta pathology in a mouse model of Alzheimer s disease 98%
- Natural genetic variation determines microglia heterogeneity in wild-derived mouse models of Alzheimer's disease 97%
- Applying high-resolution spatial transcriptomics to characterise the amyloid plaque cell niche in Alzheimer's Disease 97%
Similar papers in this journal
- DAP12 deficiency alters microglia-oligodendrocyte communication and enhances resilience against tau toxicity 98%
- β-Amyloid Induces Microglial Expression of GPC4 and APOE Leading to Increased Neuronal Tau Pathology and Toxicity 96%
- APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology 96%
Similar papers in this journal
- Diverse human astrocyte and microglial transcriptional responses to Alzheimer's pathology 97%
- Rare genetic variation in Fibronectin 1 (FN1) protects against APOEe4 in Alzheimer's disease 97%
- Dysregulated coordination of MAPT exon 2 and exon 10 splicing underlies different tau pathologies in PSP and AD 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.