Eric B. Dammer
A5054941736- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Bioinformatics and Genomic Networks
- Advanced Proteomics Techniques and Applications
- Metabolomics and Mass Spectrometry Studies
- RNA Research and Splicing
- Tryptophan and brain disorders
- Mitochondrial Function and Pathology
- S100 Proteins and Annexins
- Dementia and Cognitive Impairment Research
- Amyotrophic Lateral Sclerosis Research
- Computational Drug Discovery Methods
- RNA modifications and cancer
- Parkinson's Disease Mechanisms and Treatments
- Biotin and Related Studies
- RNA and protein synthesis mechanisms
- Neuroscience and Neuropharmacology Research
- Eicosanoids and Hypertension Pharmacology
- Machine Learning in Bioinformatics
- Ubiquitin and proteasome pathways
- RNA regulation and disease
- Cholinesterase and Neurodegenerative Diseases
- Diet and metabolism studies
- Cancer-related gene regulation
- Genetic Associations and Epidemiology
Emory University
2016-2025
Emory and Henry College
2022-2025
Institute for Neurodegenerative Disorders
2013-2024
Fundació ACE
2024
University of Iceland
2024
Icelandic Heart Association
2024
Novartis (Switzerland)
2024
Novartis Institutes for BioMedical Research
2024
Alzheimer’s Disease Neuroimaging Initiative
2024
Core Laboratories (United States)
2023
Abstract Introduction It is unclear whether abnormalities in brain glucose homeostasis are associated with Alzheimer's disease (AD) pathogenesis. Methods Within the autopsy cohort of Baltimore Longitudinal Study Aging, we measured concentration and assessed ratios glycolytic amino acids, serine, glycine, alanine to glucose. We also quantified protein levels neuronal (GLUT3) astrocytic (GLUT1) transporters. Finally, relationships between plasma before death tissue Results Higher...
Abstract Alzheimer’s disease (AD) affects half the US population over age of 85 and is universally fatal following an average course 10 years progressive cognitive disability. Genetic genome-wide association studies (GWAS) have identified about 33 risk factor genes for common, late-onset AD (LOAD), but these loci fail to account majority affected cases can neither provide clinically meaningful prediction development nor offer actionable mechanisms. This cohort study generated large-scale...
TAR DNA-binding protein 43 (TDP-43) is associated with a spectrum of neurodegenerative diseases. Although TDP-43 resembles heterogeneous nuclear ribonucleoproteins, its RNA targets and physiological partners remain unknown. Here we identify from cortical neurons by immunoprecipitation followed deep sequencing (RIP-seq). The canonical binding site (TG)n 55.1-fold enriched, moreover, variant adenine in the middle, (TG)nTA(TG)m, highly abundant among reads our RIP-seq library. can be divided...
The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood. In this study, we analyzed proteomes of more than 1,000 tissues to reveal new AD-related protein co-expression modules were highly preserved across cohorts and regions. Nearly half modules, including significantly altered AD, not observed RNA networks from same regions, highlighting proteopathic nature AD. Two such AD-associated unique proteomic network included a module related...
Disease-associated-microglia (DAM) represent transcriptionally-distinct and neurodegeneration-specific microglial profiles with unclear significance in Alzheimer's disease (AD). An understanding of heterogeneity within DAM their key regulators may guide pre-clinical experimentation drug discovery.Weighted co-expression network analysis (WGCNA) was applied to existing transcriptomic datasets from neuroinflammatory neurodegenerative mouse models identify modules highly co-expressed genes....
Abstract The availability of high-quality RNA-sequencing and genotyping data post-mortem brain collections from consortia such as CommonMind Consortium (CMC) the Accelerating Medicines Partnership for Alzheimer’s Disease (AMP-AD) enable generation a large-scale cis- eQTL meta-analysis. Here we generate cerebral cortical 1433 samples available four cohorts (identifying >4.1 million significant >18,000 genes), well cerebellar 261 874,836 >10,000 genes). We find substantially improved...
Deposition of insoluble protein aggregates is a hallmark neurodegenerative diseases. The universal presence β-amyloid and tau in Alzheimer’s disease (AD) has facilitated advancement the amyloid cascade hypotheses that have dominated AD pathogenesis research therapeutic development. However, underlying etiology remains to be fully elucidated. Here we report comprehensive study human brain-insoluble proteome by mass spectrometry. We identify 4,216 proteins, among which 36 proteins accumulate...
Alzheimer's disease (AD) lacks protein biomarkers reflective of its diverse underlying pathophysiology, hindering diagnostic and therapeutic advancements. Here, we used integrative proteomics to identify cerebrospinal fluid (CSF) representing a wide spectrum AD pathophysiology. Multiplex mass spectrometry identified ~3500 ~12,000 proteins in CSF brain, respectively. Network analysis the brain proteome resolved 44 biologically modules, 15 which overlapped with proteome. markers these...
The complicated cellular and biochemical changes that occur in brain during Alzheimer's disease are poorly understood. In a previous study we used an unbiased label-free quantitative mass spectrometry-based proteomic approach to analyze these at systems level post-mortem cortical tissue from patients with (AD), asymptomatic (AsymAD), controls. We found modules of co-expressed proteins correlated AD phenotypes, some which were enriched identified as risk factors for by genetic studies. amount...
In Alzheimer's disease (AD), spliceosomal proteins with critical roles in RNA processing aberrantly aggregate and mislocalize to Tau neurofibrillary tangles. We test the hypothesis that Tau-spliceosome interactions disrupt pre-mRNA splicing AD. human postmortem brain AD pathology, coimmunoprecipitates components. Drosophila, pan-neuronal expression triggers reductions multiple core U1-specific proteins, genetic disruption of these factors, including SmB, U1-70K, U1A, enhances Tau-mediated...
Abstract Robust and accessible biomarkers that can capture the heterogeneity of Alzheimer’s disease its diverse pathological processes are urgently needed. Here, we undertook an investigation cerebrospinal fluid (CSF) plasma from same subjects ( n= 18 control , AD) using three different proteomic platforms—SomaLogic SomaScan, Olink proximity extension assay, tandem mass tag-based spectrometry—to assess which protein markers in these two biofluids may serve as reliable AD pathophysiology...
The molecular pathology of stress-related disorders remains elusive. Our brain multiregion, multiomic study posttraumatic stress disorder (PTSD) and major depressive (MDD) included the central nucleus amygdala, hippocampal dentate gyrus, medial prefrontal cortex (mPFC). Genes exons within mPFC carried most disease signals replicated across two independent cohorts. Pathways pointed to immune function, neuronal synaptic regulation, hormones. Multiomic factor gene network analyses provided...
Abstract Dysfunction in fast-spiking parvalbumin interneurons (PV-INs) may represent an early pathophysiological perturbation Alzheimer’s Disease (AD). Defining proteomic alterations PV-INs can provide key biological and translationally-relevant insights. We used cell-type-specific in-vivo biotinylation of proteins (CIBOP) coupled with mass spectrometry to obtain native-state PV-IN proteomes. signatures include high metabolic translational activity, over-representation AD-risk cognitive...
Alzheimer’s disease (AD) is currently defined by the aggregation of amyloid-β (Aβ) and tau proteins in brain. Although biofluid biomarkers are available to measure Aβ pathology, few markers complex pathophysiology that associated with these two cardinal neuropathologies. Here, we characterized proteomic landscape cerebrospinal fluid (CSF) changes pathology 300 individuals using different technologies—tandem mass tag spectrometry SomaScan. Integration both data types allowed for generation a...
Research Article30 November 2017Open Access Transparent process A proteomic network approach across the ALS-FTD disease spectrum resolves clinical phenotypes and genetic vulnerability in human brain Mfon E Umoh Department of Neurology, Emory University School Medicine, Atlanta, GA, USA Center for Neurodegenerative Diseases, Search more papers by this author Eric B Dammer Biochemistry, Jingting Dai Duc M Duong James J Lah Allan I Levey Marla Gearing Pathology Laboratory Jonathan D Glass...