Michael T. Lardelli

tadar reduces eQTL noise in bulk RNA-sequencing by accounting for differential allelic representation during differential expression analysis.

The paper compares transcriptome and proteome changes in zebrafish models of early-onset familial Alzheimer's disease and Sanfilippo syndrome, identifying shared disease pathways.

The paper introduces a method to identify eQTLs and improve transcriptome analysis by quantifying differential allelic representation in RNA-sequencing data.

This study creates zebrafish models of MPS IIIA, IIIB, and IIIC, revealing hyperactivity, neuroinflammation, and oligodendrocyte changes similar to human disease.

The paper describes a plasmid, pHAPE, that allows the generation of DNA size markers through restriction enzyme digestions, reducing costs associated with commercial DNA ladders.

The paper examines how loss of park7 activity affects IRE gene sets in zebrafish, suggesting iron dyshomeostasis and oxidative stress may differentially impact 5' and 3' UTR IREs in Parkinson's disease.

The paper compares the effects of two PSEN1 mutations in zebrafish brains, finding distinct impacts on energy metabolism and signaling pathways linked to different diseases.

The paper compares the effects of frameshift and frame-preserving mutations in zebrafish psen2 on gene expression in young adult brains, identifying distinct cellular pathways affected.

This study investigates the effects of a SORL1 mutation in zebrafish, identifying changes in mitochondrial and ribosome function without affecting APP-related proteins or mitochondrial content.

The paper investigates the molecular effects of SORL1 mutations in zebrafish, identifying both loss- and gain-of-function impacts on brain transcriptomes related to AD.

The paper analyzes the transcriptome of zebrafish with a psen2 mutation to identify dominant effects on ribosome, mitochondrial, and anion transport functions.

This study shows that zebrafish with PSEN1 mutations exhibit accelerated hypoxia response loss with age, suggesting a link between PSEN1 dysfunction and Alzheimer's disease pathogenesis.

This study uses zebrafish embryos to develop in vivo assays investigating p75NTR and NRH1 transmembrane domain cleavage by {gamma}-secretase and related activities, revealing differential cleavage patterns.

The paper identifies IRE-containing genes and shows their expression changes are early markers of Alzheimer's disease in zebrafish, revealing species-specific differences in IRE transcript stability under iron dyshomeostasis.

This study uses a zebrafish model of familial Alzheimer’s disease to show accelerated brain aging and transcriptional inversion linked to glucocorticoid resistance and immune pathway changes before histopathology.

The paper analyzes transcriptomes of zebrafish with a familial Alzheimer's disease-like mutation in psen1, finding effects on mitochondrial ATP synthesis and ATP-dependent processes.

This paper investigates the role of zebrafish psen2 mutations in melanotic skin pigmentation, finding that specific mutations affect pigmentation without causing lethality.

The paper develops ratiometric assays in zebrafish to measure autophagic flux in models of familial Alzheimer’s disease mutations, finding altered flux in several genetic models.

The paper shows that hmga1b in zebrafish can modulate p53-dependent cellular responses but not alternative splicing of psen1, similar to hmga1a.