Duc Minh Duong

The paper compares the effects of copper deficiency in CTR1- and COX17-deficient cells using multiomics approaches, revealing distinct signaling mechanisms and proteome responses.

This paper introduces SPARO, a method to simultaneously profile transcriptomes and proteomes of neural cell types, revealing mRNA-protein discordance patterns in astrocytes and neurons.

This study identifies synaptic proteome changes in response to neuroinflammation, revealing mitochondrial and MAPK signaling disruptions in excitatory neurons linked to Alzheimer's disease.

The paper identifies five therapeutic targets for Alzheimer's disease by integrating phenotypic and proteomic screening in murine microglial cells.

This study identifies BAG3's role in astrocytic proteostasis in Alzheimer's disease by showing its interactions with autophagy, proteasome, and retromer components, and its impact on Aβ clearance.

This study develops an orthogonal ubiquitin transfer cascade to profile Parkin substrates, revealing roles in DNA replication, protein transport, and mitophagy.

The paper identifies proteomic differences in cerebrospinal fluid between sporadic and familial ALS subtypes using network analysis and validates biomarkers across neurodegenerative diseases.

The paper uses iPSC-derived astrocytes to study genetic risk factors for Alzheimer's disease, finding concordant molecular changes in both astrocytes and brain tissue.

The paper investigates how neuronal cells adapt to copper deficiency by increasing protein synthesis through mTORC1 activation and reduced PERK signaling in multiple model systems.

The paper investigates how the APOE Christchurch variant affects microglial responses to amyloid and tau pathology in mouse models, finding it enhances plaque-related responses but suppresses tau-related inflammation.

This study confirms the expression of 3R and 4R Tau isoforms and phosphorylation sites in marmoset brains, supporting their use as a model for Alzheimer's disease.

This study identifies entorhinal cortex PV interneuron vulnerability to hAPP as a driver of hyperexcitability and tau pathology in Alzheimer's Disease.

This study identifies distinct presynaptic protein networks in Lewy body dementia that differ from Alzheimer's disease using network proteomics.

This study links psychosocial experiences to mitochondrial biology in the human brain, finding positive experiences correlate with higher OxPhos machinery abundance and negative experiences with lower abundance.

The paper generates a molecular neuroanatomical map of the human prefrontal cortex using spatial transcriptomics and single nucleus RNA-sequencing, revealing novel spatial domains and cell-cell interactions linked to psychiatric disorders.

The paper shows that loss of TDP-43 function leads to the expression of de novo proteins from mis-spliced mRNA transcripts in ALS/FTD.

The paper uses heparin affinity chromatography to enrich plasma proteomes in Alzheimer's disease, identifying matrisome-associated proteins correlated with AD biomarkers.

This study shows genetic background affects the proteome in 5XFAD AD mouse models, with some disease-related modules influenced by genetic background while others are not.

The paper identifies systemic proteome and transcriptome changes in Mecp2 mutants, revealing impaired metabolic flexibility across multiple organs and brain regions.

This study shows that SORL1 loss reduces APOE levels specifically in neurons and astrocytes, linking SORL1 and APOE to Alzheimer's disease risk through distinct pathways.

The paper uses multi-platform proteomic analysis of CSF and plasma from Alzheimer's patients to identify biomarkers related to proteostasis and the matrisome.

The paper identifies shared proteomic and metabolic ontologies in Rett syndrome across species and validates them as potential biomarkers.

The paper identifies NRN1 as a mediator of cognitive resilience to Alzheimer's disease through integrative proteomic analysis and functional validation in neurons.

The paper shows that mitochondrial proteostasis genes in a neurodevelopmental syndrome locus are essential for synapse function and behavior in Drosophila.

The paper identifies pQTLs for brain proteins and finds they differ from eQTLs, suggesting distinct genetic control of mRNA and protein abundance.

This study identifies TBK1 as a tau-interacting kinase that enhances neurodegeneration in tauopathies through increased tau phosphorylation.

The paper identifies brain-linked CSF biomarkers in Alzheimer’s disease using proteomics, revealing altered levels in both brain and CSF across different disease stages.

This paper performs a large-scale eQTL meta-analysis across cerebral cortical and cerebellar brain regions, identifying distinct eQTL patterns and demonstrating improved power over existing studies.