<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Larry B. Honig</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>Columbia University</td>
</tr>
<tr>
<td class="label">Country</td>
<td>USA</td>
</tr>
<tr>
<td class="label">H-index</td>
<td>100</td>
</tr>
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<td class="label">Research Focus</td>
<td>[Alzheimer's Disease](/diseases/alzheimers), [FTD](/diseases/ftd)</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>[TDP-43](/mechanisms/tdp-43-proteinopathy), Clinical pathology</td>
</tr>
</table>
Larry B. Honig
Overview
Larry B. Honig is a leading researcher in the field of neurodegenerative diseases, affiliated with Columbia University. Their research focuses on TDP-43, Clinical pathology, with particular emphasis on Alzheimer's Disease and FTD. With an h-index of 100, Honig is among the most cited researchers in the neuroscience field[@google2026].
Honig's work spans multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Alzheimer's Disease and FTD. Their research group has made significant contributions to the fields of TDP-43, Clinical pathology, publishing in high-impact journals including leading neuroscience journals.
...<table class="infobox infobox-researcher">
<tr>
<th class="infobox-header" colspan="2">Larry B. Honig</th>
</tr>
<tr>
<td class="infobox-image" colspan="2">
<em>Photo placeholder</em>
</td>
</tr>
<tr>
<td class="label">Affiliations</td>
<td>Columbia University</td>
</tr>
<tr>
<td class="label">Country</td>
<td>USA</td>
</tr>
<tr>
<td class="label">H-index</td>
<td>100</td>
</tr>
<tr>
<td class="label">Research Focus</td>
<td>[Alzheimer's Disease](/diseases/alzheimers), [FTD](/diseases/ftd)</td>
</tr>
<tr>
<td class="label">Mechanisms</td>
<td>[TDP-43](/mechanisms/tdp-43-proteinopathy), Clinical pathology</td>
</tr>
</table>
Larry B. Honig
Overview
Larry B. Honig is a leading researcher in the field of neurodegenerative diseases, affiliated with Columbia University. Their research focuses on TDP-43, Clinical pathology, with particular emphasis on Alzheimer's Disease and FTD. With an h-index of 100, Honig is among the most cited researchers in the neuroscience field[@google2026].
Honig's work spans multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Alzheimer's Disease and FTD. Their research group has made significant contributions to the fields of TDP-43, Clinical pathology, publishing in high-impact journals including leading neuroscience journals.
Based at Columbia University, Honig 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)
- [FTD](/diseases/ftd)
Mechanisms of Interest
- TDP-43
- Clinical pathology
Programmatic Emphasis
Honig's portfolio emphasizes mechanism-aware biomarker interpretation and translational hypothesis testing in Alzheimer's Disease and FTD[@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 TDP-43, Clinical pathology 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
[PubMed author search for Larry B. Honig](https://pubmed.ncbi.nlm.nih.gov/?term=Larry+B.+Honig%5BAuthor%5D)[@google2026]
[Google Scholar author search for Larry B. Honig](https://scholar.google.com/scholar?q=author%3A%22Larry+B.+Honig%22)[@google2026]
[Semantic Scholar profile search for Larry B. Honig](https://www.semanticscholar.org/search?q=Larry+B.+Honig)[@google2026]
Recent Research
Recent PubMed-indexed publications (2024-present):
[Predictive Value of Plasma P-tau217 and APOE Genotype for Preclinical Cognitive Decline in Alzheimer's Disease.](https://pubmed.ncbi.nlm.nih.gov/41728301/). medRxiv : the preprint server for health sciences. 2026.
[Polygenic scores of Core 1 Alzheimer's disease biomarkers predict early cognitive and pathological change.](https://pubmed.ncbi.nlm.nih.gov/41307156/). Alzheimer's & dementia : the journal of the Alzheimer's Association. 2025.
[Evaluating polygenic risk score prediction performance for Alzheimer's disease in a population-based Hispanic cohort using single- and multi-ancestry models.](https://pubmed.ncbi.nlm.nih.gov/40747112/). Lancet regional health. Americas. 2025.
[Polygenic Scores of Core-1 Alzheimer's Disease Biomarkers Predict Early Cognitive and Pathological Change.](https://pubmed.ncbi.nlm.nih.gov/40791715/). medRxiv : the preprint server for health sciences. 2025.
Collaborators and Research Network
Collaborator network pending enrichment.
Institutional Context
Primary institutional links: [Columbia University](/institutions/columbia-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 TDP-43, Clinical pathology 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 and FTD into clinically meaningful interventions?
External Links
- Google Scholar: [Search for Larry B. Honig](https://scholar.google.com/scholar?q=author%3A%22Larry+B.+Honig%22)
- PubMed: [Author search for Larry B. Honig](https://pubmed.ncbi.nlm.nih.gov/?term=Larry+B.+Honig%5BAuthor%5D)
See Also
- [Researchers and Institutions Index](/researchers)
- [Diseases Index](/diseases)
- [Mechanisms Index](/mechanisms)
References
Unknown, Google Scholar author search for Larry B. Honig (2026)
[Unknown, Long and Holtzman, Alzheimer disease an update on pathobiology and treatment strategies 2019 (2019)](https://pubmed.ncbi.nlm.nih.gov/30617256/)