Tara L. Spires‐Jones

The paper uses polygenic risk scores to analyze genetic contributions to neurodegenerative diseases across brain cell types, finding shared and disease-specific genetic risks.

The paper identifies early synaptic vesicle cycle disruption in ALS using proteomics and shows it is reversible with TDP-43 suppression.

This study establishes an adult-onset Drosophila model of tauopathy, revealing sex-specific effects on survival and behavior and identifying genetic modifiers of tau-induced dysfunction.

This study shows that increased somatodendritic Tau interacts with nuclear envelope proteins, causing nuclear damage and altering gene expression related to AD and tauopathies.

This study examines amyloid-beta pathology in feline cognitive dysfunction syndrome, finding increased synaptic engulfment by glia in aged and affected cats, mirroring Alzheimer's disease mechanisms.

This study uses live human brain slice cultures to show that physiological and pathological amyloid-beta have opposing effects on synapses, with physiological levels enhancing synaptic transcripts and pathological levels causing synaptic loss.

The paper conducts a Bayesian EWAS and GWAS of smoking using DNA methylation data from blood and brain tissues, identifying smoking-related loci and developing an epigenetic biomarker.

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.

The paper shows Drosophila melanogaster resist trans-synaptic spread of human tau, suggesting they are not suitable for screening tau propagation modifiers.

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.

This study shows that retaining proteins in the ER can rescue Aβ toxicity in Drosophila and mouse models, suggesting a potential therapeutic strategy for Alzheimer's disease.

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 identifies truncated Aβ fragments that form SDS-stable, low molecular weight oligomers impairing synaptic plasticity and evading conventional antibodies.

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.

This study shows reducing Kv3.4 levels in a mouse model of Alzheimer's disease reduces synapse loss and changes in spine morphology.

This study shows that higher plasma phospho-tau181 levels and their increase over time predict faster cognitive decline in older adults and are present in brain synapses.

This study shows that reducing tau with a degrader prevents mitochondrial fragmentation and oxidative stress in ALS models.

This study shows that loss of SORCS2 increases DNA double-strand breaks in neurons, linking it to neurodegenerative processes.

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.

This study uses MRI and histology to identify structural and cellular changes in TDP-43 knock-in mice, linking them to ALS-FTD pathology and identifying PV+ interneuron loss as a potential biomarker.

The paper develops a DNA methylation-based proxy for interleukin-6 and finds it correlates with age and cognitive functioning better than serum IL-6.

This study identifies nutrient signaling pathways that regulate amyloid clearance and synaptic loss in Alzheimer's disease, showing both protective and harmful effects.

This paper investigates whether demyelination in multiple sclerosis leads to selective neurodegeneration of inhibitory interneurons and presents a rodent model to study this phenomenon.

This study examines C9orf72 ALS/FTD patient-derived iPSC-microglia mono-cultures, finding they form RNA foci, have reduced C9orf72 protein, and show endosomal-lysosomal dysfunction, but no significant microglial-enriched gene expression differences.

The paper develops an epigenetic CRP score to assess chronic inflammation and its link to cognitive ability, finding it more consistently associated with cognition than serum CRP across two cohorts.

The paper investigates microglial synaptic internalisation in schizophrenia post-mortem brains and finds no differences in microglial activation or pre-synaptic protein levels between schizophrenia and control cases.

This paper introduces DNAm GrimAge, an epigenetic clock that predicts mortality and is associated with multiple brain health measures in older adults.

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.