Professor, Neurology, Brigham and Women's Hospital, Harvard Medical School
Neurology
Dr. Dennis J. Selkoe, MD
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Dr. Dennis J. Selkoe practices Neurology. He researched medicine at University of Virginia School of Medicine. He received 3 awards: "Elected Member", "Super Doctor" and "Whos Who in Medicine and Healthcare". Dennis Selkoe is a published physician. He published 102 publications, including: 'A critical appraisal of the pathogenic protein spread hypothesis of neurodegeneration.' He accepts all Medicare patients.
Publications
- Fluorescent Analogue of Batimastat Enables Imaging of α-Secretase in Living Cells.
- Soluble Aβ oligomers impair hippocampal LTP by disrupting glutamatergic/GABAergic balance.
- C-Terminally Truncated Forms of Tau, But Not Full-Length Tau or Its C-Terminal Fragments, Are Released from Neurons Independently of Cell Death.
- Association between α-synuclein blood transcripts and early, neuroimaging-supported Parkinson's Disease.
- Purification of α-Synuclein from Human Brain Reveals an Instability of Endogenous Multimers as the Protein Approaches Purity.
- Pen-2 Is Essential for γ-Secretase Complex Stability and Trafficking but Partially Dispensable for Endoproteolysis.
- γ-Secretase: A Horseshoe Structure Brings Good Luck.
- Genetic deletion of the GATA1-regulated protein α-synuclein reduces oxidative stress and nitric oxide synthase levels in mature erythrocytes.
- Functional analysis and purification of a Pen-2 fusion protein for γ-secretase structural studies.
- Soluble Aβ Oligomers Are Rapidly Sequestered from Brain ISF In Vivo and Bind GM1 Ganglioside on Cellular Membranes.
- The familial Alzheimer's Disease APPV717I mutation alters APP processing and Tau expression in iPSC-derived neurons.
- SnapShot: Pathobiology of Alzheimer's Disease.
- Systematic Evaluation of Candidate Ligands Regulating Ectodomain Shedding of Amyloid Precursor Protein.
- Environmental Novelty Activates ?2-Adrenergic Signaling to Prevent the Impairment of Hippocampal LTP by A? Oligomers.
- In Vivo Cross-linking Reveals Principally Oligomeric Forms of ?-Synuclein and ?-Synuclein in Neurons and Non-neural Cells.
- New ELISAs with high specificity for soluble oligomers of amyloid ?-protein detect natural A? oligomers in human brain but not CSF.
- Discovery of a novel pharmacological and structural class of gamma secretase modulators derived from the extract of Actaea racemosa.
- Pancortins interact with amyloid precursor protein and modulate cortical cell migration.
- Preventing Alzheimer's Disease.
- Effects of membrane lipids on the activity and processivity of purified γ-secretase.
- Recommendations for the incorporation of biomarkers into Alzheimer clinical trials: an overview.
- Dynamic Analysis of Amyloid ?-Protein in Behaving Mice Reveals Opposing Changes in ISF versus Parenchymal A? during Age-Related Plaque Formation.
- Cholesterol Level and Statin Use in Alzheimer Disease: II. Review of Human Trials and Recommendations.
- Cholesterol level and statin use in Alzheimer Disease: I. Review of epidemiological and preclinical studies.
- Association of SNCA with Parkinson: replication in the Harvard NeuroDiscovery Center Biomarker Study.
- ?-Synuclein neuropathology is controlled by nuclear hormone receptors and enhanced by docosahexanoic acid in a mouse model for Parkinson's Disease.
- ?-Synuclein occurs physiologically as a helically folded tetramer that resists aggregation.
- Alzheimer's Disease.
- Soluble A{beta} Oligomers Inhibit Long-Term Potentiation through a Mechanism Involving Excessive Activation of Extrasynaptic NR2B-Containing NMDA Receptors.
- Plasma beta-amyloid level, cognitive reserve, and cognitive decline.
- Relation Between Insulin, Insulin-related Factors, and Plasma Amyloid Beta Peptide Levels at Midlife in a Population-based Study.
- Soluble amyloid {beta}-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.
- Resolving controversies on the path to Alzheimer's therapeutics.
- Isolation of low-n amyloid β-protein oligomers from cultured cells, CSF, and brain.
- Biochemical and functional interaction of disrupted-in-schizophrenia 1 and amyloid precursor protein regulates neuronal migration during mammalian cortical development.
- Giving Alzheimer's the old one-two.
- Aph-1 associates directly with full-length and C-terminal fragments of gamma-secretase substrates.
- Functional alterations in memory networks in early Alzheimer's Disease.
- Abeta oligomers inhibit synapse remodelling necessary for memory consolidation.
- Designed inhibitors of insulin-degrading enzyme regulate the catabolism and activity of insulin.
- Biochemical and immunohistochemical analysis of an Alzheimer's Disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.
- Ten-year change in plasma amyloid beta levels and late-life cognitive decline.
- HLA-DR alleles in amyloid beta-peptide autoimmunity: a highly immunogenic role for the DRB1*1501 allele.
- Amyloid deposition is associated with impaired default network function in older persons without Dementia.
- Toward structural elucidation of the gamma-secretase complex.
- Pink1 forms a multiprotein complex with Miro and Milton, linking Pink1 function to mitochondrial trafficking.
- Evidence that alpha-synuclein does not inhibit phospholipase D.
- A specific enzyme-linked immunosorbent assay for measuring beta-amyloid protein oligomers in human plasma and brain tissue of patients with Alzheimer Disease.
- Identification of beta-secretase (BACE1) substrates using quantitative proteomics.
- Small-molecule activators of insulin-degrading enzyme discovered through high-throughput compound screening.
- Proteomic profiling of gamma-secretase substrates and mapping of substrate requirements.
- Aggregation and catabolism of Disease-associated intra-Abeta mutations: reduced proteolysis of AbetaA21G by neprilysin.
- Direct and potent regulation of gamma-secretase by its lipid microenvironment.
- Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory.
- Molecular basis for the thiol sensitivity of insulin-degrading enzyme.
- Amyloid beta protein dimer-containing human CSF disrupts synaptic plasticity: prevention by systemic passive immunization.
- LRP promotes endocytosis and degradation, but not transcytosis, of the amyloid-beta peptide in a blood-brain barrier in vitro model.
- A critical function for beta-amyloid precursor protein in neuronal migration revealed by in utero RNA interference.
- Developing preventive therapies for chronic Diseases: lessons learned from Alzheimer's Disease.
- Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells.
- Soluble Abeta inhibits specific signal transduction cascades common to the insulin receptor pathway.
- Presenilin: running with scissors in the membrane.
- Reducing amyloid plaque burden via ex vivo gene delivery of an Abeta-degrading protease: a novel therapeutic approach to Alzheimer Disease.
- Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathy.
- Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid beta-protein metabolism in mouse models of Alzheimer Disease.
- Decreased catalytic activity of the insulin-degrading enzyme in chromosome 10-linked Alzheimer Disease families.
- Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway.
- Response to: Pardossi-Piquard et al., "Presenilin-Dependent Transcriptional Control of the Abeta-Degrading Enzyme Neprilysin by Intracellular Domains of betaAPP a...
- Orally available compound prevents deficits in memory caused by the Alzheimer amyloid-beta oligomers.
- Alterations in memory networks in mild cognitive impairment and Alzheimer's Disease: an independent component analysis.
- The ups and downs of Abeta.
- Electron microscopic structure of purified, active gamma-secretase reveals an aqueous intramembrane chamber and two pores.
- gamma-Secretase substrate selectivity can be modulated directly via interaction with a nucleotide-binding site.
- Amyloid beta-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor.
- Small non-fibrillar assemblies of amyloid beta-protein bearing the Arctic mutation induce rapid neuritic degeneration.
- Dopamine covalently modifies and functionally inactivates parkin.
- By the way, doctor. Is there a brain scan that can specifically diagnose Alzheimer's Disease?
- Physiological regulation of the beta-amyloid precursor protein signaling domain by c-Jun N-terminal kinase JNK3 during neuronal differentiation.
- Alternative splicing of human insulin-degrading enzyme yields a novel isoform with a decreased ability to degrade insulin and amyloid beta-protein.
- Amyloid beta protein immunotherapy neutralizes Abeta oligomers that disrupt synaptic plasticity in vivo.
- Certain inhibitors of synthetic amyloid beta-peptide (Abeta) fibrillogenesis block oligomerization of natural Abeta and thereby rescue long-term potentiation.
- Gamma-secretase exists on the plasma membrane as an intact complex that accepts substrates and effects intramembrane cleavage.
- Defining molecular targets to prevent Alzheimer Disease.
- Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function.
- Deciphering the molecular basis of memory failure in Alzheimer's Disease.
- Purification and characterization of the human gamma-secretase complex.
- Alzheimer's Disease abeta vaccine reduces central nervous system abeta levels in a non-human primate, the Caribbean vervet.
- A seed for Alzheimer amyloid in the brain.
- Partial loss-of-function mutations in insulin-degrading enzyme that induce diabetes also impair degradation of amyloid beta-protein.
- Block of long-term potentiation by naturally secreted and synthetic amyloid beta-peptide in hippocampal slices is mediated via activation of the kinases c-Jun N-termin...
- Detergent-dependent dissociation of active gamma-secretase reveals an interaction between Pen-2 and PS1-NTF and offers a model for subunit organization within the comp...
- Inhibition of receptor-mediated endocytosis demonstrates generation of amyloid beta-protein at the cell surface.
- Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death.
- Altered fatty acid composition of dopaminergic neurons expressing alpha-synuclein and human brains with alpha-synucleinopathies.
- Functional gamma-secretase complex assembly in Golgi/trans-Golgi network: interactions among presenilin, nicastrin, Aph1, Pen-2, and gamma-secretase substrates.
- Aging, amyloid, and Alzheimer's Disease: a perspective in honor of Carl Cotman.
- Evidence for peripheral clearance of cerebral Abeta protein following chronic, active Abeta immunization in PSAPP mice.
- Kinetics of amyloid beta-protein degradation determined by novel fluorescence- and fluorescence polarization-based assays.
- A critical appraisal of the pathogenic protein spread hypothesis of neurodegeneration.
- Nicastrin functions to sterically hinder γ-secretase-substrate interactions driven by substrate transmembrane domain.
- New insights into cellular α-synuclein homeostasis in health and Disease.
Schools
Virginia Commonwealth University School Of Medicine
Hospital Of The University Of Pennsylvania
Pb BrighamChldns HospBeth
Chldns Hospital Med Center
Conditions Treated
- Alzheimer's Disease
- Dementia
Doctors Specialties
- Neurology
Accepted Insurances
Awards
- Elected Member
- Super Doctor
- Whos Who in Medicine and Healthcare
Education
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Boston Children's Hospital -
Beth Israel Deaconess Medical Center -
University of Pennsylvania Health System -
University of Virginia School of Medicine
Hospital
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Brigham and Women's Hospital
Drug Facts
| NPI NUMBER | 1184614356 | |
| NPPES Provider LastName | SELKOE | |
| NPPES Provider FirstName | DENNIS | |
| NPPES Provider ZIPCode | 021155727 | |
| NPPES Provider State | MA | |
| Specialty Description | Neurology | |
| Total Claim Count | 87.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1184614356 |
| Last Name Of The Provider | SELKOE |
| First Name Of The Provider | DENNIS |
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