<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Stanley B. Prusiner</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>University of California, San Francisco</td>
</tr>
<tr>
<td class="label">Country</td>
<td>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/0000-0001-7218-6255" target="_blank">0000-0001-7218-6255</a></td>
</tr>
<tr>
<td class="label">Research Focus</td>
<td>[Prion Disease](/diseases/prion-diseases), Alzheimer Disease, Parkinson Disease</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>Prions, Protein Misfolding, [Amyloid](/mechanisms/amyloid-cascade), [Neurodegeneration](/mechanisms/neurodegeneration)</td>
</tr>
</table>
Stanley B. Prusiner
Overview
Stanley B. Prusiner is a leading researcher in the field of neurodegenerative diseases, affiliated with University of California, San Francisco. Their research focuses on Prions, Protein Misfolding, Amyloid, Neurodegeneration, with particular emphasis on Prion Disease and Alzheimer Disease and Parkinson Disease. With an h-index of 200, Prusiner is among the most cited researchers in the neuroscience field[@orcid2026].
...<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Stanley B. Prusiner</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>University of California, San Francisco</td>
</tr>
<tr>
<td class="label">Country</td>
<td>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/0000-0001-7218-6255" target="_blank">0000-0001-7218-6255</a></td>
</tr>
<tr>
<td class="label">Research Focus</td>
<td>[Prion Disease](/diseases/prion-diseases), Alzheimer Disease, Parkinson Disease</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>Prions, Protein Misfolding, [Amyloid](/mechanisms/amyloid-cascade), [Neurodegeneration](/mechanisms/neurodegeneration)</td>
</tr>
</table>
Stanley B. Prusiner
Overview
Stanley B. Prusiner is a leading researcher in the field of neurodegenerative diseases, affiliated with University of California, San Francisco. Their research focuses on Prions, Protein Misfolding, Amyloid, Neurodegeneration, with particular emphasis on Prion Disease and Alzheimer Disease and Parkinson Disease. With an h-index of 200, Prusiner is among the most cited researchers in the neuroscience field[@orcid2026].
Prusiner's work spans multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Prion Disease and Alzheimer Disease and Parkinson Disease. Their research group has made significant contributions to the fields of Prions, Protein Misfolding, Amyloid, Neurodegeneration, publishing in high-impact journals including Cell.
Based at University of California, San Francisco, Prusiner collaborates with researchers across multiple institutions worldwide, working to advance therapeutic strategies for neurodegenerative conditions.
Research Focus
Disease Areas
- [Prion Disease](/diseases/prion-diseases)
- Alzheimer Disease
- Parkinson Disease
Mechanisms of Interest
- Prions
- Protein Misfolding
- [Amyloid](/mechanisms/amyloid-cascade)
- [Neurodegeneration](diseases/neurodegeneration)
Programmatic Emphasis
Prusiner's portfolio emphasizes mechanism-aware biomarker interpretation and translational hypothesis testing in Prion Disease and Alzheimer Disease and Parkinson 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 Prions, Protein Misfolding, Amyloid, Neurodegeneration 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
[Novel proteinaceous infectious particles causing scrapie](https://doi.org/10.1016/0092-8674(82)90552-4). Cell, 1982.[@novel1982]
Recent Research
No clearly attributable PubMed-indexed neuroscience publications were found for 2024-present in this cycle.
- [PubMed live search](https://pubmed.ncbi.nlm.nih.gov/?term=Stanley+B.+Prusiner+2024%3A3000%5Bdp%5D+%28brain+OR+neuron+OR+neurodegenerative%29)
Collaborators and Research Network
Collaborator network pending enrichment.
Institutional Context
Primary institutional links: [University of California, San Francisco](/institutions/university-of-california-san-francisco). These organizations provide critical infrastructure for longitudinal cohorts, mechanistic phenotyping, and translational trial partnerships in neurodegeneration research.
Open Questions and Future Directions
- How can Prions, Protein Misfolding, Amyloid, Neurodegeneration 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 Prion Disease and Alzheimer Disease and Parkinson Disease into clinically meaningful interventions?
External Links
- ORCID: [https://orcid.org/0000-0001-7218-6255](https://orcid.org/0000-0001-7218-6255)
- Google Scholar: [Search for Stanley B. Prusiner](https://scholar.google.com/scholar?q=author%3A%22Stanley+B.+Prusiner%22)
- PubMed: [Author search for Stanley B. Prusiner](https://pubmed.ncbi.nlm.nih.gov/?term=Stanley+B.+Prusiner%5BAuthor%5D)
See Also
- [Researchers and Institutions Index](/researchers)
- [Diseases Index](/diseases)
- [Mechanisms Index](/mechanisms)
References
[Unknown, Novel proteinaceous infectious particles causing scrapie (1982)](https://doi.org/10.1016/0092-8674(82)
Unknown, ORCID profile for Stanley B. Prusiner (2026)