Frances Wiseman

Publications

• Mouse models of aneuploidy.
• A genetic cause of Alzheimer disease: Mechanistic insights from Down syndrome
• Replication-timing boundaries facilitate cell-type and species-specific regulation of a rearranged human chromosome in mouse
• Gene expression dysregulation domains are not a specific feature of Down syndrome.
• Cathepsin B abundance, activity and microglial localisation in Alzheimer’s disease – Down syndrome and early onset Alzheimer’s disease; the role of elevated cystatin B
• Generation of a panel of antibodies against proteins encoded on human chromosome 21
• The role of host PrP in Transmissible Spongiform Encephalopathies
• Altered glycosylated PrP proteins can have different neuronal trafficking in brain but do not acquire scrapie-like properties
• Glycosylation and misfolding of PrP
• Overexpression of the Hspa13 (Stch) gene reduces prion disease incubation time in mice
• Protein profiles in Tc1 mice implicate novel pathway perturbations in the down syndrome brain
• The glycosylation status of PrPC is a key factor in determining transmissible spongiform encephalopathy transmission between species
• Massively Parallel Sequencing Reveals the Complex Structure of an Irradiated Human Chromosome on a Mouse Background in the Tc1 Model of Down Syndrome
• Automatic structural parcellation of mouse brain MRI using multi-atlas label fusion
• Structural correlates of active-staining following magnetic resonance microscopy in the mouse brain
• Cognitive Enhancement Therapy for a Model of Down Syndrome
• Down syndrome and the molecular pathogenesis resulting from trisomy of human chromosome 21
• Grey matter sublayer thickness estimation in the mouse cerebellum
• Fully-automated |JMRI morphometric phenotyping of the Tc1 mouse model of down syndrome
• Changing Paradigms in Down Syndrome: The First International Conference of the Trisomy 21 Research Society
• Down syndrome - Recent progress and future prospects
• Mouse models of aneuploidy
• The integration site of the APP transgene in the J20 mouse model of Alzheimer’s disease
• Altered regulation of tau phosphorylation in a mouse model of down syndrome aging
• Tc1 mouse model of trisomy-21 dissociates properties of short- and long-term recognition memory
• Plasma biomarkers for amyloid, tau, and cytokines in Down syndrome and sporadic Alzheimer's disease.
• Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP.
• T1, diffusion tensor, and quantitative magnetization transfer imaging of the hippocampus in an Alzheimer's disease mouse model.
• Analysis of motor dysfunction in Down Syndrome reveals motor neuron degeneration.
• Downregulated Wnt/β-catenin signalling in the Down syndrome hippocampus.
• Genetic mapping of APP and amyloid-β biology modulation by trisomy 21
• Publisher Correction: Genetic dissection of down syndrome‑associated alterations in APP/amyloid‑β biology using mouse models.
• Building the Future Therapies for Down Syndrome: The Third International Conference of the T21 Research Society.
• Endosomal structure and APP biology are not altered in a preclinical mouse cellular model of Down syndrome
• A novel knockout mouse for the small EDRK-rich factor 2 (Serf2) showing developmental and other deficits.
• Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models.
• The effects ofCSTBduplication on APP/amyloid-β pathology and cathepsin activity in a mouse model
• Genetic dissection of Down syndrome-associated alterations in APP/amyloid-β biology using mouse models
• Altered Hippocampal-Prefrontal Neural Dynamics in Mouse Models of Down Syndrome.
• Using mouse models to understand Alzheimer's disease mechanisms in the context of trisomy of chromosome 21.
• Altered Hippocampal-Prefrontal Neural Dynamics in Mouse Models of Down Syndrome
• Rodent Modeling of Alzheimer's Disease in Down Syndrome: In vivo and ex vivo Approaches.
• Genetic Mapping of APP and Amyloid-β Biology Modulation by Trisomy 21.
• Cathepsin B abundance, activity and microglial localisation in Alzheimer’s disease-Down syndrome and early onset Alzheimer’s disease; the role of elevated cystatin B
• Substantially thinner internal granular layer and reduced molecular layer surface in the cerebellar cortex of the Tc1 mouse model of down syndrome – a comprehensive morphometric analysis with active staining contrast-enhanced MRI
• Cell models for Down syndrome-Alzheimer’s disease research
• Endosomal structure and APP biology are not altered in preclinical cellular models of Down syndrome
• The integration site of the APP transgene in the J20 mouse model of Alzheimer's disease.
• The effects of Cstb duplication on APP/amyloid-β pathology and cathepsin B activity in a mouse model
• Reduction of Cystatin B results in increased cathepsin B activity in disomic but not Trisomy21 human cellular and mouse models
• SynPull: a novel method for studying neurodegeneration-related aggregates in synaptosomes using super-resolution microscopy
• Reduction of Cystatin B results in increased cathepsin B activity in disomic but not Trisomy 21 human cellular and mouse models