Area of research
Neurology · Physiology
Research interest
Research interests include Alzheimer's disease research and treatments, Parkinson's Disease Mechanisms and Treatments, Prion Diseases and Protein Misfolding, and Neurological diseases and metabolism.
Astrocytes from P301S Tau mice exhibit non-canonical protein secretion and reduced morphological complexity.
Early α-synuclein–mediated mitochondrial dysfunction in a human cell model of Parkinson’s disease dementia
Proteomizer: Leveraging the Transcriptome-Proteome Mismatch to Infer Novel Gene Regulatory Relations
Alpha-synuclein aggregation and dopaminergic neuron death in a new mouse model of Parkinson’s disease expressing human full-length and C-terminally truncated 1- 120 alpha-synuclein
GhostBuster: A Deep-Learning-based, Literature-Unbiased Gene Prioritization Tool for Gene Annotation Prediction
Alpha-synuclein pathological deposition alters functional homeostasis and connectivity of striatal dopaminergic synapses and results in microglia activation, pathology spreading, muscle stiffness, whole brain atrophy and metabolic changes before producing frank nigral neuron deafferentation
The pathogenesis of Parkinson's disease
α-Synuclein oligomers form by secondary nucleation
Aging, Parkinson’s Disease, and Models: What Are the Challenges?
Targeting tau degradation: a viable therapeutic approach?
Synapsin III gene silencing redeems alpha-synuclein transgenic mice from Parkinson's disease-like phenotype
Cryo-EM reconstruction of TMEM106B fold I-d filaments from case 18 with multiple system atrophy
Microglia become hypofunctional and release metalloproteases and tau seeds when phagocytosing live neurons with P301S tau aggregates.
Preclinical development of a high affinity α-synuclein antibody, MEDI1341, that can enter the brain, sequester extracellular α-synuclein and attenuate α-synuclein spreading in vivo
Depopulation of dense α-synuclein aggregates is associated with rescue of dopamine neuron dysfunction and death in a new Parkinson's disease model.
Retiring the term FTDP-17 as MAPT mutations are genetic forms of sporadic frontotemporal tauopathies
Regional expression of the MAPT gene is associated with loss of hubs in brain networks and cognitive impairment in Parkinson disease and progressive supranuclear palsy
The role of tau in the pathological process and clinical expression of Huntington’s disease
Tau pathology and neurodegeneration
100 years of Lewy pathology
Animal models of Parkinson's disease: Limits and relevance to neuroprotection studies
Mechanisms underlying the impairment of hippocampal long-term potentiation and memory in experimental Parkinson’s disease
Mixed tau, TDP-43 and p62 pathology in FTLD associated with a C9ORF72 repeat expansion and p.Ala239Thr MAPT (tau) variant