<table class="infobox infobox-researcher">
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<th class="infobox-header" colspan="2">Dennis J. Selkoe</th>
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<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
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<td class="label">Affiliations</td>
<td>Brigham and Women's Hospital<br>Harvard Medical School</td>
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<td class="label">Country</td>
<td>USA</td>
</tr>
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<td class="label">H-index</td>
<td>250</td>
</tr>
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<td class="label">ORCID</td>
<td><a href="https://orcid.org/0000-0001-9469-1830" target="_blank">0000-0001-9469-1830</a></td>
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<td class="label">Research Focus</td>
<td>[Alzheimer's Disease](/diseases/alzheimers)</td>
</tr>
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<td class="label">Mechanisms</td>
<td>[Amyloid](/mechanisms/amyloid-cascade), [APP processing](/mechanisms/app-processing), [Synaptic plasticity](/mechanisms/synaptic-dysfunction-ad)</td>
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Dennis J. Selkoe
Overview
Dennis J. Selkoe is a leading researcher in the field of neurodegenerative diseases, affiliated with Brigham and Women's Hospital and Harvard Medical School. Their research focuses on Amyloid, APP processing, Synaptic plasticity, with particular emphasis on Alzheimer's Disease. With an h-index of 250, Selkoe is among the most cited researchers in the neuroscience field[@orcid2026].
...<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Dennis J. Selkoe</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>Brigham and Women's Hospital<br>Harvard Medical School</td>
</tr>
<tr>
<td class="label">Country</td>
<td>USA</td>
</tr>
<tr>
<td class="label">H-index</td>
<td>250</td>
</tr>
<tr>
<td class="label">ORCID</td>
<td><a href="https://orcid.org/0000-0001-9469-1830" target="_blank">0000-0001-9469-1830</a></td>
</tr>
<tr>
<td class="label">Research Focus</td>
<td>[Alzheimer's Disease](/diseases/alzheimers)</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>[Amyloid](/mechanisms/amyloid-cascade), [APP processing](/mechanisms/app-processing), [Synaptic plasticity](/mechanisms/synaptic-dysfunction-ad)</td>
</tr>
</table>
Dennis J. Selkoe
Overview
Dennis J. Selkoe is a leading researcher in the field of neurodegenerative diseases, affiliated with Brigham and Women's Hospital and Harvard Medical School. Their research focuses on Amyloid, APP processing, Synaptic plasticity, with particular emphasis on Alzheimer's Disease. With an h-index of 250, Selkoe is among the most cited researchers in the neuroscience field[@orcid2026].
Selkoe's work spans multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Alzheimer's Disease. Their research group has made significant contributions to the fields of Amyloid, APP processing, Synaptic plasticity, publishing in high-impact journals including Nat Rev Neurosci, Neuron.
Based at Brigham and Women's Hospital and Harvard Medical School, Selkoe collaborates with researchers across multiple institutions worldwide, working to advance therapeutic strategies for neurodegenerative conditions.
Research Focus
Disease Areas
- [Alzheimer's Disease](/diseases/alzheimers-disease)
Mechanisms of Interest
- [Amyloid](/mechanisms/amyloid-cascade)
- [APP processing](/mechanisms/app-processing)
- [Synaptic plasticity](/mechanisms/synaptic-dysfunction)
Programmatic Emphasis
Selkoe's portfolio emphasizes mechanism-aware biomarker interpretation and translational hypothesis testing in Alzheimer's Disease[@long2019]. Their group typically links molecular process readouts to clinically meaningful outcomes, including cognitive trajectories, motor phenotypes, and disease staging endpoints when relevant.
The work frequently sits at the interface of discovery science and implementation, using study designs that can be transferred from observational cohorts to interventional studies. This makes the profile especially relevant for NeuroWiki pages that connect molecular mechanisms to treatment strategy, trial design, and patient stratification.
Methods and Data Strategy
Within the Amyloid, APP processing, Synaptic plasticity domain, this research profile is most aligned with multimodal integration: combining imaging, biofluid, genomic, and clinical metadata to derive robust disease signatures. In practice, this means prioritizing reproducibility (cohort harmonization, independent replication, and transparent analysis assumptions) over one-off findings.
The program also supports comparative interpretation across related disorders, helping distinguish disease-general stress biology from disease-specific pathomechanisms. That distinction is important for mechanistic ranking and for selecting therapeutic targets with realistic translational potential.
Translational Relevance
For NeuroWiki readers, the translational value of this researcher profile lies in three areas: first, operationalizing mechanism-informed biomarkers for diagnosis and progression tracking; second, identifying patient subgroups most likely to respond to targeted interventions; and third, connecting preclinical hypotheses to trial-ready outcome frameworks.
This orientation improves actionability of mechanistic knowledge graphs because it links entities and pathways to measurable clinical decisions. Pages connected to this profile should therefore prioritize explicit mechanism-to-outcome chains, with clear assumptions and evidence quality labels.
Key Publications
[Soluble oligomers of amyloid beta](https://doi.org/10.1016/S0896-6273(02)00752-0). Neuron, 2002.[@soluble2002]
[Amyloid beta as a pathogen in Alzheimer's disease](https://doi.org/10.1038/nrn1226). Nat Rev Neurosci, 2003.[@amyloid2003]
Recent Research
Recent PubMed-indexed publications (2025-present):
[Higher-molecular-weight a-synuclein oligomers are increased in the brain cytosol of patients with dementia with Lewy bodies.](https://pubmed.ncbi.nlm.nih.gov/41764273/). NPJ Parkinson's disease. 2026.
[Parkinson disease is a fatty acidopathy.](https://pubmed.ncbi.nlm.nih.gov/41034503/). Nature reviews. Neurology. 2025.
[The case for regulatory approval of amyloid-lowering immunotherapies in Alzheimer's disease based on clearcut biomarker evidence.](https://pubmed.ncbi.nlm.nih.gov/39535341/). Alzheimer's & dementia : the journal of the Alzheimer's Association. 2025.
Collaborators and Research Network
[John Hardy](/researchers/john-hardy), [Reisa A. Sperling](/researchers/reisa-sperling), [David M. Holtzman](/researchers/david-holtzman), [Michael S. Wolfe](/researchers/michael-wolfe)
Institutional Context
Primary institutional links: [Brigham and Women's Hospital](/institutions/brigham-and-women's-hospital), [Harvard Medical School](/institutions/harvard-medical-school). These organizations provide critical infrastructure for longitudinal cohorts, mechanistic phenotyping, and translational trial partnerships in neurodegeneration research.
Open Questions and Future Directions
- How can Amyloid, APP processing, Synaptic plasticity signals be standardized across cohorts and sites without losing disease-stage sensitivity?
- Which biomarker combinations best separate causal mechanism activity from downstream epiphenomena?
- What trial designs can most efficiently translate mechanistic findings in Alzheimer's Disease into clinically meaningful interventions?
External Links
- ORCID: [https://orcid.org/0000-0001-9469-1830](https://orcid.org/0000-0001-9469-1830)
- Google Scholar: [Search for Dennis J. Selkoe](https://scholar.google.com/scholar?q=author%3A%22Dennis+J.+Selkoe%22)
- PubMed: [Author search for Dennis J. Selkoe](https://pubmed.ncbi.nlm.nih.gov/?term=Dennis+J.+Selkoe%5BAuthor%5D)
See Also
- [Researchers and Institutions Index](/researchers)
- [Diseases Index](/diseases)
- [Mechanisms Index](/mechanisms)
References
[Unknown, Soluble oligomers of amyloid beta (2002)](https://doi.org/10.1016/S0896-6273(02)
[Unknown, Amyloid beta as a pathogen in Alzheimer's disease (2003)](https://doi.org/10.1038/nrn1226)
Unknown, ORCID profile for Dennis J. Selkoe (2026)
[Unknown, Long and Holtzman, Alzheimer disease an update on pathobiology and treatment strategies 2019 (2019)](https://pubmed.ncbi.nlm.nih.gov/30617256/)