Anita Bhattacharyya

This study uses single-nucleus multiomic sequencing to analyze gene expression and chromatin accessibility in the Down syndrome prefrontal cortex, revealing widespread dysregulation in metabolic, synaptic, and neuroinflammatory pathways.

This study shows that Leucettinib-21 reduces DYRK1A activity in human trisomy 21 neural cells, supporting its potential as a therapeutic for Down syndrome.

The paper uses single-nucleus sequencing to identify oxidative stress and metabolic changes in Down syndrome basal forebrain neurons at birth.

Directly-reprogrammed human neurons show reduced neurite growth ability with age, mirroring rodent developmental patterns.

This study identifies reduced WNT signaling in Down syndrome progenitors, leading to fewer COUP-TFII+ interneurons and impaired neurogenesis.

The paper develops a chemical cocktail to induce senescence in iPSC-derived neurons to better model age-related neurodegenerative disorders.

This paper introduces a CRISPR/Cas9 strategy to edit APP and manipulate the amyloid pathway in Alzheimer's disease by reducing β-cleavage and Aβ while increasing α-cleavage.