Valina Lynn Dawson

This paper maps α-synuclein pathology and dopaminergic degeneration in mice using multimodal imaging and microscopy, showing spread along the nigrostriatal pathway and microstructural changes.

This study shows that gut-to-brain propagation of alpha-synuclein fibrils induces REM sleep behavior disorder and other non-motor and motor Parkinson's disease phenotypes.

This study identifies a mechanism by which reactive astrocytes drive neurodegeneration in synucleinopathies through extracellular acidification and neuronal ASIC1a activation.

This study identifies microglial Lag3 as a key receptor linking extracellular α-synuclein PFF recognition to neurotoxic astrocyte conversion and dopaminergic neurodegeneration.

This study shows that PARIS in neurons activates STAT3, leading to tau pathology and glial activation in Alzheimer's disease, and identifies the PARIS-STAT3 pathway as a therapeutic target.

This study shows PARP1 inhibition reduces amyloid pathology, neurodegeneration, and cognitive decline in a mouse model of Alzheimer's disease.

The paper shows a copper-containing nanozyme worsens alpha-synucleinopathy by increasing nitrosative stress, while a copper-free version reduces pathology in neurodegenerative models.

This study identifies a spatially organized IGF1-mTOR signaling mechanism in human forebrain progenitors that regulates proliferation and fate through transcriptional and translational control.

This study shows that APOE genotype affects neurovascular vulnerability in human forebrain organoids under viral stress, with APOE2/2 and APOE4/4 showing distinct inflammatory and vascular responses.

This study uses HiF-snRNA-seq to analyze the cingulate cortex in Parkinson's disease and Parkinson's disease dementia, identifying cell-type-specific gene expression changes and disease-stage-related pathways.

This study shows neuronal LAG3 is essential for α-synuclein propagation and neurodegeneration in Parkinson's disease, suggesting LAG3 as a therapeutic target.

The paper determines the cryo-EM structure of Thorase filaments, showing how ATP binding drives filament formation and provides insights into its role in disassembling mTORC1 complexes.

The paper identifies distinct α-synuclein strains associated with cognitive decline in Parkinson's disease and shows AI-based analysis of these strains improves clinical stratification.

This study shows that alpha-synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons, leading to bioenergetic deficits and neuronal dysfunction in Parkinson's disease.

The paper identifies a deficient PAR response in Huntington disease patients, suggesting a potential therapeutic target for early intervention.

This study investigates how PARP-1 activation and PAR binding to HK-1 impair glycolysis, mitochondrial function, and redox balance in neurons under oxygen-glucose deprivation.

This paper identifies NOD2/RIPK2 signaling as a key driver of neuroinflammation in Parkinson's disease, showing that pathological α-synuclein activates this pathway in microglia, leading to neurodegeneration and that targeting NOD2 or RIPK2 protects dopamine neurons.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

This study shows that defects in mitochondrial biogenesis, not mitophagy, are the primary cause of mitochondrial alterations in PINK1-deficient human dopamine neurons.

This study identifies that pathological α-synuclein destabilizes the TSC1-TSC2 complex, activates mTORC1, and enhances protein translation, contributing to neurodegeneration in Parkinson's disease.

This paper introduces Cal-ID, a tool that records calcium signaling and neuronal activity by biotinylating nearby proteins, enabling high-resolution molecular mapping.

The paper identifies neuroprotective compounds for retinitis pigmentosa using cross-species drug screens in zebrafish and mouse models, finding additive effects in some combinations.

The paper identifies complement and coagulation cascade pathways as significantly altered in two Parkinson's disease mouse models through proteome analysis.

The paper identifies Aplp1 and its complex with Lag3 as facilitators of pathologic alpha-synuclein transmission and toxicity, showing that disrupting this complex prevents neurodegeneration.

The paper identifies ACE2-expressing endothelial and mural cells in mouse brains and links their functional changes to age-related vulnerability to viral infection.

The paper establishes the landscape of human cell-specific microRNA expression using small RNA-seq data from diverse cell types and tissues, identifying novel microRNA loci and patterns correlated with super-enhancer activity.

The paper introduces TRiP, a method for cell type-specific ribosome profiling, and shows experience-induced changes in translation in mouse CA1 pyramidal cells.