Leslie Michels Thompson

The paper generates isogenic iPSC lines with CAG repeats and HTT KO for Huntington's disease study, showing differentiation potential and altered gene expression in neurons and astrocytes.

This paper evaluates combining expression-based surrogate variables and genotype-based principal components in differential expression analysis, finding the combined approach improves replicability and biological recall in ALS datasets.

This paper develops a multimodal spatial transcriptomics approach to study CAG repeat expansion, huntingtin aggregation, and neuron loss in Huntington's Disease using human brain tissue.

This study identifies epigenetic biomarkers in cell-free DNA for ALS diagnosis and progression prediction using methylation analysis.

The paper identifies strategies to prevent transgene silencing during human pluripotent stem cell differentiation and introduces a robust vector construct.

This study uses single-nucleus multi-omics to identify shared and distinct regulatory pathways in Pick's and Alzheimer's disease, revealing disease-specific enhancers and TF binding patterns.

The paper investigates TDP-43 SUMOylation and its role in DNA damage repair under oxidative stress.

The paper introduces the Neurolipid Atlas, a lipidomics resource for neurodegenerative diseases, revealing that ApoE4 impairs astrocyte reactivity by promoting cholesterol ester accumulation.

The paper shows that Huntingtin (HTT) helps maintain mitochondrial DNA integrity by organizing a repair complex, which is disrupted by mutant HTT in Huntington's disease, leading to DNA damage and motor deficits in a fly model.

This study compares the effects of HTT knockout and CAG repeat expansion in cortical neurons, identifying shared and distinct biological pathways involved in HD.

The paper identifies a deficient PAR response in Huntington disease patients, suggesting a potential therapeutic target for early intervention.

This study identifies a mechanism where HTT recruits BRG1 and NHEJ components to repair transcription-associated DSBs in neurons, and shows that mutant HTT impairs this process, contributing to HD pathology.

This paper introduces EpiOut, a tool to detect chromatin accessibility outliers in ALS, showing they correlate with gene expression and protein level aberrations.

This study shows that BDNF and TRiC-inspired reagents can rescue synaptic deficits in HD mouse models.

This study identifies TDP-43 dysfunction and reduced m6A modification as mechanisms causing aberrant splicing in Huntington's disease using mouse and human brain data.

The paper analyzes ATAC-seq data from iPSC-derived motor neurons of ALS patients and controls to identify disease-specific chromatin accessibility changes and their predictive power for disease progression.

This study uses cryoET and proteomics to identify mitochondrial and organelle abnormalities in HD models, showing potential for early diagnosis and therapy development.

This study compares HD astrocytes from human iPSCs and mouse models, identifying dysregulated synaptogenesis, actin signaling, and maturation, with unique human findings and potential therapeutic targets.

This study uses snRNAseq to analyze HD mouse models and human brain tissue, identifying impaired oligodendrocyte maturation and a potential role for thiamine metabolism in disease pathology.

The paper compares TDP-43's transcriptional and splicing effects in muscle and neuronal cells, showing tissue-specific roles in disease.

This study shows that human neural stem cells transplanted into Huntington's disease mouse models improve behavior, reduce mutant Huntingtin, and integrate functionally into the host brain.

The paper performs an integrated multi-omic analysis of iPSC-derived motor neurons from C9ORF72 ALS patients to identify dysregulated pathways and validate them in vivo and in postmortem data.

The paper uses unsupervised machine learning to identify three molecular subtypes in ALS cortex samples, associated with oxidative stress, retrotransposon activation, and glial activation.

This study compares 3-DGE and conventional mRNAseq, finding similar gene expression results with 3-DGE offering cost savings and scalability.