Owen Dando

The paper investigates how loss of FMRP in a rat model of FXS affects functional connectivity over development and whether early lovastatin treatment can normalize it.

The paper compares two iPSC-microglia protocols to assess how the MAPT-S305N mutation affects microglial function and neuronal health in a frontotemporal dementia model.

This study examines the association between APOE4 genotype, BBB permeability, and infarct distribution in patients with mild ischemic stroke, finding a posterior-predominant infarct distribution in APOE4 carriers despite similar BBB metrics.

The paper identifies NRF2 activation in mononuclear myeloid cells as a protective response to intracerebral haemorrhage, showing its therapeutic potential through modulation of interferon pathways.

This study shows astrocytes alter the transcriptomic and epigenetic landscape of developing cortical neurons, promoting intrinsic excitability and influencing disease-related pathways.

The paper investigates how ASD mutations in CEP41 affect cortical neuron development in human organoids, finding altered cilia stability and changes in interneuron and projection neuron differentiation.

This study identifies pericyte loss preceding endothelial activation in cerebral small vessel disease through single-vessel analysis of human brain tissue.

This study shows that LTP in sensory cortex is impaired in Fragile X mice, leading to hypoplasticity in layer 2/3 pyramidal neurons and altered somatosensory processing.

This study investigates the cell-type-specific role of Nrf2 in regulating transcriptional signatures and inflammatory responses in the adult mouse brain.

This study shows that C9ORF72-mutant astrocytes disrupt axonal transport in motor neurons, and correcting this rescues transport deficits.

This paper shows that endothelial cell Nrf2 activation reduces neuroinflammation caused by systemic inflammation.

This study investigates the role of FMRP in oligodendrocyte maturation and myelination in human and rat models, finding shared defects in morphology and function.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

This study shows that neurodevelopmental processes in the cortex and thalamus can occur normally without microglia, using a genetically modified mouse model.

This study shows microglia promote beta-amyloid plaque formation but are not required for subsequent pathological changes in Alzheimer's disease.

The paper identifies transmembrane protein 97 as a synaptic receptor for amyloid beta in human Alzheimer's disease using advanced microscopy and drug intervention studies.

This study investigates the sex-specific role of Cst7 in microglia in an amyloid-driven Alzheimer's Disease model, finding sexually dimorphic effects on endolysosomal function and inflammation.

The paper shows that astrocyte-oligodendrocyte interaction is critical for remyelination and identifies a drug strategy targeting this interaction to promote central nervous system regeneration.

The paper identifies two distinct neuroinflammatory signatures in ALS cohorts using gene expression analysis and validates their association with clinical metrics.

The paper compares human and mouse exon usage in cortical neurons, finding conservation in basal inclusion but divergence in activity-dependent usage, suggesting both cis-acting and trans-acting factors contribute to species differences.

This study shows that rats with Fragile X Syndrome exhibit impaired experience-dependent changes in hippocampal spatial activity and circuit function compared to wild-type rats.

The paper examines flight-freeze response imbalances in Nlgn3-/y rats, finding hyperexcitability in periaqueductal grey neurons linked to altered fear behaviors.

The paper identifies excessive ribosomal protein translation as a key factor in Fragile X Syndrome by showing its role in disrupting synaptic protein translation and LTD.

The paper identifies developing interneurons as a potential target for autism genetic risk factors by analyzing human and rodent neural data.

LAB-AID is an interactive web tool that visualizes and interrogates hierarchical biological experimental data to improve understanding and identify outliers and batch effects.

This study shows that loss of FMRP in a mouse model of Fragile X Syndrome leads to increased single-spine excitation and more multiply-innervated spines, contributing to circuit hyperexcitability.

The paper investigates the impact of a t(1;11) translocation on white matter integrity and oligodendrocyte-myelin function using DTI and cellular models.

This study shows that reducing tau improves behavioural and transcriptional issues in a mouse model of Alzheimer’s disease, suggesting synaptic tau reduction could be a therapeutic strategy.