Anita Adami

The paper investigates TE transcription in Parkinson's disease brains, finding region- and cell-type-specific TE activation linked to an interferon response in microglia and neurons.

This paper describes a protocol for CRISPRi-mediated silencing of retrotransposons in hiPSCs, validated using a multiome approach combining RNA-seq, CUT&RUN, and proteomics.

This study shows that loss of H3K9me3 in human neural progenitor cells activates L1 retrotransposons by reducing CpG methylation at their promoters.

This study identifies a chimpanzee-specific retroviral insertion that influences gene regulation and brain development, highlighting its role in human-chimpanzee brain divergence.

This study maps cell-type specific transcriptional changes in the parkinsonian striatum across species, identifying vulnerable and resilient cell types.

The paper develops cell-type-specific transcriptomic aging clocks using single-nuclei RNA sequencing data from human prefrontal cortex tissue, showing distinct aging patterns across cell types.

This study shows that L1 retrotransposons influence human pluripotency exit and early brain development through their expression and derived transcripts.

This study shows MORC2 regulates CpG methylation of active LINE-1 retrotransposons during human neurodevelopment, similar to the piRNA pathway in the germline.

This study develops a method to efficiently generate human oligodendrocytes from induced pluripotent stem cells, which can form functional myelinating grafts in adult human brain tissue.

The paper shows that DNA methylation and the HUSH-MORC2 complex independently regulate repeat elements in human neural progenitor cells, with MORC2 binding increasing in demethylated regions.

The paper shows that sequencing ambiguity between GBA1 and its pseudogene GBAP1 affects transcriptomic analysis, revealing non-lysosomal functions in the brain and widespread annotation inaccuracies.

This study shows L1 retrotransposons contribute to human brain transcriptome complexity and functional diversification through cell-type specific transcripts and regulatory RNAs.

The paper shows that ZNF91 creates mini-heterochromatin domains that limit the regulatory impact of SVA transposons in human neural progenitor cells, contributing to XDP pathology.

The paper uses snRNA-seq to analyze TBI brain tissue, finding oligodendroglia activate endogenous retroviruses, linking them to neuroinflammation.