Morgan Newman

PRESENILIN 1 mutations causing early-onset familial Alzheimer's disease or familial acne inversa differ in their effects on genes facilitating energy metabolism and signal transduction

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.

Transcriptome analyses of 7-day-old zebrafish larvae possessing a familial Alzheimer's disease-like mutation in psen1 indicate effects on oxidative phosphorylation, mcm functions, and iron homeostasis

Frameshift and frame-preserving mutations in zebrafish presenilin 2 affect different cellular functions in young adult brains

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.

Comparative analysis of Alzheimer's disease knock-in model brain transcriptomes implies changes to energy metabolism as a causative pathogenic stress

Transcriptome analysis of a protein-truncating mutation in sortilin-related receptor 1 associated with early-onset familial Alzheimer's disease indicates effects on mitochondrial and ribosome function in young-adult zebrafish brains

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.

Brain transcriptome analysis reveals subtle effects on mitochondrial function and iron homeostasis of mutations in the SORL1 gene implicated in early onset familial Alzheimers disease

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.

Transcriptome analysis indicates dominant effects on ribosome and mitochondrial function of a premature termination codon mutation in the zebrafish gene psen2

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

Accelerated loss of hypoxia response in zebrafish with familial Alzheimer's disease-like mutation of Presenilin 1.

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.

Developing in vivo assays for investigation of p75NTR and NRH1 transmembrane domain cleavage events using zebrafish embryos

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.

Iron Responsive Element (IRE)-mediated responses to iron dyshomeostasis in Alzheimer's disease

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.

Accelerated brain aging towards transcriptional inversion in a zebrafish model of familial Alzheimer’s disease

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.

A familial Alzheimer's disease-like mutation in the zebrafish presenilin 1 gene affects brain energy production

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.

The zebrafish orthologue of familial Alzheimer’s disease gene PRESENILIN 2 is required for normal adult melanotic skin pigmentation

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

Ratiometric assays of autophagic flux in zebrafish for analysis of familial Alzheimer’s disease-like mutations

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.

HMGA1 zebrafish co-orthologue hmga1b can modulate p53-dependent cellular responses but is unable to control the alternative splicing of psen1

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