<table class="infobox infobox-researcher">
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<th class="infobox-header" colspan="2">Thomas C. Südhof</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
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<td class="label">Affiliations</td>
<td>Stanford University</td>
</tr>
<tr>
<td class="label">Country</td>
<td>Germany/USA</td>
</tr>
<tr>
<td class="label">H-index</td>
<td>200</td>
</tr>
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<td class="label">ORCID</td>
<td><a href="https://orcid.org/0000-0002-0923-0988" target="_blank">0000-0002-0923-0988</a></td>
</tr>
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<td class="label">Research Focus</td>
<td>Neuropsychiatric Disorders, Alzheimer Disease</td>
</tr>
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<td class="label">Mechanisms</td>
<td>Synaptic Transmission, SNARE Complex, Synaptotagmin</td>
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Thomas C. Südhof
Overview
Thomas C. Südhof is a leading researcher in the field of neurodegenerative diseases, affiliated with Stanford University. Their research focuses on Synaptic Transmission, SNARE Complex, Synaptotagmin, with particular emphasis on Neuropsychiatric Disorders and Alzheimer Disease. With an h-index of 200, Südhof is among the most cited researchers in the neuroscience field[@orcid2026].
...<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Thomas C. Südhof</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>Stanford University</td>
</tr>
<tr>
<td class="label">Country</td>
<td>Germany/USA</td>
</tr>
<tr>
<td class="label">H-index</td>
<td>200</td>
</tr>
<tr>
<td class="label">ORCID</td>
<td><a href="https://orcid.org/0000-0002-0923-0988" target="_blank">0000-0002-0923-0988</a></td>
</tr>
<tr>
<td class="label">Research Focus</td>
<td>Neuropsychiatric Disorders, Alzheimer Disease</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>Synaptic Transmission, SNARE Complex, Synaptotagmin</td>
</tr>
</table>
Thomas C. Südhof
Overview
Thomas C. Südhof is a leading researcher in the field of neurodegenerative diseases, affiliated with Stanford University. Their research focuses on Synaptic Transmission, SNARE Complex, Synaptotagmin, with particular emphasis on Neuropsychiatric Disorders and Alzheimer Disease. With an h-index of 200, Südhof is among the most cited researchers in the neuroscience field[@orcid2026].
Südhof's work spans multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Neuropsychiatric Disorders and Alzheimer Disease. Their research group has made significant contributions to the fields of Synaptic Transmission, SNARE Complex, Synaptotagmin, publishing in high-impact journals including Nature.
Based at Stanford University, Südhof collaborates with researchers across multiple institutions worldwide, working to advance therapeutic strategies for neurodegenerative conditions.
Research Focus
Disease Areas
- Neuropsychiatric Disorders
- Alzheimer Disease
Mechanisms of Interest
- [Synaptic Transmission](/mechanisms/synaptic-dysfunction) SNARE Complex
- Synaptotagmin
Programmatic Emphasis
Südhof's portfolio emphasizes mechanism-aware biomarker interpretation and translational hypothesis testing in Neuropsychiatric Disorders and Alzheimer Disease. 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 Synaptic Transmission, SNARE Complex, Synaptotagmin 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
[Synaptotagmin I as a Ca2+ sensor](https://doi.org/10.1038/357647a0). Nature, 1992.[@synaptotagmin1992]
Recent Research
Recent PubMed-indexed publications (2024-present):
[Distinct mechanisms control the specific synaptic functions of Neuroligin 1 and Neuroligin 2.](https://pubmed.ncbi.nlm.nih.gov/39747663/). EMBO reports. 2025.
[Generation of human excitatory forebrain neurons by cooperative binding of proneural NGN2 and homeobox factor EMX1.](https://pubmed.ncbi.nlm.nih.gov/38446849/). Proceedings of the National Academy of Sciences of the United States of America. 2024.
Collaborators and Research Network
[James E. Rothman](/researchers/james-rothman)
Institutional Context
Primary institutional links: [Stanford University](/institutions/stanford-university). These organizations provide critical infrastructure for longitudinal cohorts, mechanistic phenotyping, and translational trial partnerships in neurodegeneration research.
Open Questions and Future Directions
- How can Synaptic Transmission, SNARE Complex, Synaptotagmin 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 Neuropsychiatric Disorders and Alzheimer Disease into clinically meaningful interventions?
External Links
- ORCID: [https://orcid.org/0000-0002-0923-0988](https://orcid.org/0000-0002-0923-0988)
- Google Scholar: [Search for Thomas C. Südhof](https://scholar.google.com/scholar?q=author%3A%22Thomas+C.+Südhof%22)
- PubMed: [Author search for Thomas C. Südhof](https://pubmed.ncbi.nlm.nih.gov/?term=Thomas+C.+S%C3%BCdhof%5BAuthor%5D)
See Also
- [Researchers and Institutions Index](/researchers)
- [Diseases Index](/diseases)
- [Mechanisms Index](/mechanisms)
References
[Unknown, Synaptotagmin I as a Ca2+ sensor (1992)](https://doi.org/10.1038/357647a0)
Unknown, ORCID profile for Thomas C. Südhof (2026)