Derek H. Oakley

The paper introduces multiDIA, a proteomics method that improves sequence coverage and scalability in neurodegenerative disease studies by combining multiple proteases and data-independent acquisition.

The paper uses single-nucleus RNA-seq to analyze cerebrovascular transcriptomic changes in Alzheimer's Disease and primary tauopathies, identifying shared heat-shock responses and disease-specific vascular remodeling.

This study presents a single-cell multi-omic atlas of Alzheimer's disease brain regions, revealing region-specific epigenomic changes and altered cell states.

The paper identifies rare bioactive tau oligomers in Alzheimer's brain that can induce templated misfolding and fibril formation, distinguishing them from non-bioactive oligomers.

This paper uses micro-XRD and XRF to analyze tau aggregates in Pick's disease, finding distinct elemental compositions and fibril structures in different lesion types.

This study identifies proteomic changes in Alzheimer's disease, revealing decreased 20S proteasome levels and altered ubiquitin system enzymes contributing to protein accumulation.

The paper examines somatic mutations in neurons across tau pathologic states in Alzheimer's disease and finds increased mutation burden and specific mutational signatures in AD neurons.

The paper develops open-source tools for 3D analysis of brain dissection photographs and surface scans, achieving accurate reconstructions and segmentations comparable to MRI.

The paper uses natural language processing on post-mortem electronic health records to derive RDoC cognitive scores and associates them with Alzheimer's disease neuropathology.

The paper correlates DNA methylation patterns between buccal and brain samples to identify CpG sites with significant methylation correlations and genetic determinants.

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