Eric B. Dammer

This study uses proteomics to identify aging and Aβ-related molecular changes in mouse brains and finds they are conserved in human AD proteomes.

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 194 miRNAs with widespread changes in Alzheimer's disease, including novel miRNAs not previously linked to AD, revealing new biological pathways and suggesting AD may be a systemic disorder.

The paper identifies RNA-binding proteins interacting with tau's repeat domain using proximity labeling, showing their enrichment in Alzheimer's and tauopathies.

The paper identifies six CSF proteomic subtypes in Alzheimer's disease, linking BBB dysfunction to reduced tau and synaptic biomarkers, particularly in African Americans and men.

The paper identifies cross-species biomarkers and mechanisms in Rett Syndrome using gene therapy and multi-omic analysis in mice.

This study identifies chronic neuroinflammation in MS through scRNA-seq and proteomics, showing persistent IFN signaling and CD8 T cell cytotoxicity despite B-cell depletion.

This study identifies molecular subtypes based on cryptic exon burden in hippocampal tissue, revealing proteomic changes linked to TDP-43 pathology in LATE and Alzheimer's disease.

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 performs large-scale proteomic analysis of Alzheimer's disease brain regions across different racial and ethnic groups, identifying AD-related protein changes and APOE4 concordance with genotype.

This paper presents a multi-omics dataset from multi-ethnic Alzheimer's disease brain donors, including transcriptome, genome, and proteome data, to improve precision medicine for underrepresented populations.

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

The paper identifies a conserved Aβ amyloid 'responsome' in human and mouse AD brains, showing how amyloid scaffolds proteins involved in disease pathology.

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 finds reduced PIN1 gene expression in female Alzheimer's patients correlates with cognitive decline and neuropathological features, suggesting it as a potential biomarker for AD risk in women.

The paper compares proteomic profiles of cerebrospinal fluid from African Americans and Caucasians with and without Alzheimer's disease to identify shared and divergent biomarkers.

This study examines how repeated mild traumatic brain injuries affect the brain in 3xTg mice, identifying sex-specific changes in gene expression and immune responses.

The paper uses TurboID-NES to profile proteomes of microglial and neuronal cell lines, showing it captures a significant portion of the proteome and responds to LPS treatment.

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 uses proteomic profiling to classify cognitive impairment subtypes in human brain tissues, identifying distinct molecular patterns associated with different clinical outcomes.

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

This study shows that candesartan improves learning and working memory in female TgF344-AD rats but not males, through mechanisms involving clusterin and GFAP, independent of blood pressure or amyloid-β changes.

The paper identifies a cell-type specific signature of cognitive resilience to Alzheimer's disease in human and mouse models, highlighting excitatory intratelencephalic cortical neurons and several resilience genes.

The paper analyzes proteomic data from Alzheimer's disease brains, revealing disease-related changes not seen at the RNA level and identifying potential therapeutic targets.

This study identifies ERK phosphorylation in microglia as a critical regulator of pro-inflammatory responses in Alzheimer’s disease using pre-clinical models and human proteomic data.

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.