Glenda Margaret Halliday

This study identifies a bidirectional pathogenic relationship between alpha-synuclein and neuromelanin in Parkinson's disease, showing they promote each other's accumulation and neuronal loss.

The paper identifies astrocytes as a key site of dsRNA accumulation and ADAR1 p150 induction in Parkinson's disease, linking dsRNA sensing to complement activation in a cell-type-specific manner.

This study shows that astrocytes in the substantia nigra pars compacta of A53T transgenic mice have more -synuclein aggregates and reactive morphology compared to wild-type mice.

This study identifies Netrin-1 as a DA-specific cue that enhances graft integration and functional recovery in Parkinsonian models without off-target effects.

The paper identifies and maps GABAergic cell clusters in the human rostromedial tegmental nucleus (RMTg) and retrorubral fields (RRF) using immunohistochemistry and anatomical staining.

The paper identifies BCL-XL as a potential regulator of the neurovascular unit in Parkinson's disease through systematic screening of -Synuclein strain responses in pericytes.

This study uses patient-derived tau aggregates to induce disease-specific tauopathy features in human cells, revealing distinct pathological responses across tau strains.

The paper uses machine learning to analyze neuronal morphology in Parkinson's disease iPSC-derived neurons, identifying genotype-specific mitochondrial and lysosomal abnormalities.

This study generates CHCHD2 T61I mutant mice to model Parkinson's disease, finding mitochondrial dysfunction and metabolic shifts towards glycolysis.

This study identifies region-specific vascular changes in Parkinson's disease brains, showing reduced aquaporin-4 and increased string vessels correlate with disease duration.

This paper standardises and automates the quantification of intracellular neuromelanin granules in human brain tissue sections using TruAI, revealing age-related changes in their properties.

This study compares dopamine and cortical neurons with PD mutations to identify cellular dysfunctions linked to different pathological phenotypes.

This study identifies genetic risk factors for FTLD-TDP subtypes using whole-genome sequencing and meta-analysis across multiple cohorts.

The paper introduces MJF-14 PLA, a proximity ligation assay for detecting non-inclusion alpha-synuclein aggregates with high specificity and sensitivity, showing pathology precedes Lewy body formation in Parkinson's disease.

This paper develops an iPSC platform to rapidly generate alpha-synuclein inclusions and investigates their formation, subtypes, and molecular interactions.

This study shows that chronic hyperactivation of midbrain dopamine neurons leads to their preferential degeneration, suggesting increased neural activity may contribute to Parkinson's disease pathology.

Peripheral blood-derived cells can be employed to stratify Parkinson's disease patients most likely to respond to LRRK2-related therapeutics.

The paper introduces a single-cell DNA methylation sequencing method that improves resolution and accuracy compared to existing techniques.

This study develops a programmable nanopore sequencing assay for diagnosing all known pathogenic STRs in a single test, accurately diagnosing 27 patients with neurogenetic disorders.

This paper identifies five new genetic risk loci for Lewy body dementia through whole-genome sequencing and shows shared risk profiles with Alzheimer’s and Parkinson’s disease.

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.

This study profiles RNA expression in MSA cerebellar tissue, identifying distinct transcriptional signatures between parkinsonian and cerebellar subtypes, with greater dysregulation observed in the cerebellar subtype.

The paper identifies novel non-coding RNAs in human brain tissue associated with neuropsychiatric traits using targeted RNA capture and long-read sequencing.

This study estimates the heritability of dementia with Lewy bodies (DLB) and finds it to be higher than previous estimates, with low variance explained by polygenic risk scores from Parkinson's or Alzheimer's disease.

This study examines how dopamine depletion affects large-scale brain network dynamics in Parkinson's disease by comparing network integration in patients On and Off dopamine therapy with healthy controls.

The paper improves age prediction from DNA methylation using larger datasets, showing reduced error and limitations in capturing biological ageing variation.

The paper identifies a genetic variant near CXCR4 associated with increased risk for PSP and PD, showing dysregulation of CXCR4 and microglia-related genes in neurodegenerative diseases.