Colin Smith

This study identifies spatially resolved aging and senescence signatures in the human hippocampus using multi-omics approaches, revealing cell-type and sex-specific gene expression changes.

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.

The paper maps cognitive impairments in ALS by integrating spatial and single-nucleus transcriptomics, revealing distinct cellular and molecular patterns in language and executive dysfunction.

This study uses multi-omics data to compare molecular signatures in the motor cortex and lumbar spinal cord of ALS patients, finding distinct alterations in MN and glial functions depending on symptom onset site.

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.

The paper identifies disease-specific molecular profiles of small tau aggregates across different tauopathies using single-molecule assays.

This study shows that systemic FAK inhibition reduces immunosuppressive macrophages in glioblastoma by blocking monocyte trafficking, enhancing T cell activity and improving survival in a mouse model.

The paper examines SV2A expression in synapses across mouse and human brains, revealing regional and synaptic variability that challenges current PET imaging interpretations.

This study identifies TDP-43-driven splicing dysregulation as a common mechanism in ALS, FTD, and Alzheimer's disease, linking them through mis-spliced mRNAs like APP.

The paper identifies senescent cell signatures in the human dorsolateral prefrontal cortex using spatial transcriptomics and single nucleus RNA sequencing, revealing heterogeneity and cell-type-specific aging patterns.

This study identifies heterozygous lysosomal enzyme gene mutations as risk factors for Alzheimer's disease and validates their impact on amyloid-beta processing using mouse models.

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.

The paper shows human astrocytes and microglia ingest more synapses in Alzheimer's disease via MFG-E8, and inhibiting MFG-E8 reduces this ingestion in cultured cells.

This study shows that C9orf72 mutations disrupt autophagy in microglia, leading to immune dysfunction and increased motor neuron death in ALS/FTD.

This paper identifies diverse brain microbes in health and disease, finding over-represented pathogens in Alzheimer's brain samples.

This study compares DNA methylation signatures of ageing and inflammation in blood and brain tissues, finding divergent correlations and a link between epigenetic age acceleration and microglial burdens in the hippocampus.

The paper investigates tripartite synapse loss in ALS models and human tissue, finding selective vulnerability of these synapses in both mice and humans.

The paper applies blood-derived epigenetic predictors of lifestyle traits to brain samples, finding variable correlations across brain regions and a strong link between smoking and the dorsolateral prefrontal cortex.

The paper maps the human synaptome, finding conserved synaptic features between humans and mice despite evolutionary divergence.

The paper identifies over 5,500 synaptic proteins in Alzheimer’s disease and controls, revealing APOE4-associated changes in synaptic and mitochondrial function and neuroimmune signaling.

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 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.