Ashutosh Dhingra

The paper investigates transcriptomic changes in oligodendroglial lineage cells from PD patient-iPSCs with LRRK2-G2019S mutation, identifying altered pathways and signaling in OPCs and ODCs.

This study evaluates AAV transduction efficiency and toxicity across human iPSC-derived neuronal subtypes, identifying optimal serotypes for gene delivery in vitro.

The paper investigates how the H1/H1 risk allele at the MAPT locus increases susceptibility to mild chronic oxidative stress in iNeurons and identifies FDA-approved compounds that rescue this vulnerability.

This study shows that iPSC-derived neurons from FTD patients exhibit synaptic dysfunction, DNA damage, and C9-HRE-related pathologies, supporting synaptic dysfunction as a key factor in FTD.

The paper shows that an ATTTC repeat insertion in an Alu element enhances a DAB1 enhancer, leading to neuronal dysfunction in SCA37.

This study shows that C9orf72 repeat expansion in iPSC-derived microglia from FTD patients leads to increased phagocytic activity and reduced autophagosomal-lysosomal vesicles.

The paper identifies transcription factors that regulate β-glucocerebrosidase activity, showing that USF2 and ONECUT2 have opposing effects on GCase levels and function.

The paper presents a multi-omics dataset for genetic subtypes of frontotemporal dementia to identify molecular mechanisms disrupted in the disease.

The paper constructs genome-wide CRISPR libraries for gene ablation, activation, and silencing with high efficacy and reports novel gene regulators and modifiers.

This paper identifies 54 novel regulators of PrPC expression through a genome-wide RNA interference screen, with 9 confirmed by CRISPR interference, revealing potential therapeutic targets for prion diseases.