Progranulin deficiency in the brain activates an insulin signaling pathway that may promote neurodegeneration.
Overview
- Division of Endocrinology and Metabolism, Department of Internal Medicine, University of South Florida Morsani College of Medicine, Tampa, FL 33602, USA
- Tampa Veterans Administration Medical Center, Tampa, FL 33612, USA
- Division of Geriatric Medicine, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104, USA
- Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 63104, USA
- Institute for Translational Neuroscience, Saint Louis University, St. Louis, MO 63104, USA
- Department of Chemistry, University of South Florida School of Arts and Sciences, Tampa, FL 33620, USA
Abstract
Molecular mechanisms in frontotemporal dementia (FTD) and Alzheimer’s disease (AD) are obscure. FTD can result from loss-of-function progranulin mutations, although pathogenetic consequences are uncertain. Progranulin insufficiency also increases human AD risk, and progranulin treatment improves mouse AD. Furthermore, AD and FTD risks are abetted by obesity/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
The paper's code and data availability statement is in the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data and code availability
• All data generated in this study are included in the article. • This paper does not report original code. • Any additional information required to reanalyze the data reported in this paper is available from the lead contact upon request.
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 29 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 9 authors, 3 keywords, 5 funders, 129 references, 27 RRIDs.
Cite
This paper
Sajan, M. P., Aggarwal, G., Hwang, J. J., Smith, D. M., Cooper, D. R., Duncan, M. A., Hansen, B. C., Nguyen, A. D., & Farese, R. V. (2026). Progranulin deficiency in the brain activates an insulin signaling pathway that may promote neurodegeneration. iScience, 29(5), 115720. https://
BibTeX
@article{sajan2026progra
author = {Sajan, Mini P. and Aggarwal, Geetika and Hwang, Joel Jihwan and Smith, Denise M. and Cooper, Denise R. and Duncan, Mildred Acevedo and Hansen, Barbara C. and Nguyen, Andrew D. and Farese, Robert V.},
title = {{Progranulin deficiency in the brain activates an insulin signaling pathway that may promote neurodegeneration}},
journal = {iScience},
year = {2026},
month = apr,
volume = {29},
number = {5},
pages = {115720},
publisher = {Elsevier},
issn = {2589-0042},
doi = {10.1016/
url = {https://
pmid = {42095076},
pmcid = {PMC13141651}
}
RIS
TY - JOUR
AU - Sajan, Mini P.
AU - Aggarwal, Geetika
AU - Hwang, Joel Jihwan
AU - Smith, Denise M.
AU - Cooper, Denise R.
AU - Duncan, Mildred Acevedo
AU - Hansen, Barbara C.
AU - Nguyen, Andrew D.
AU - Farese, Robert V.
TI - Progranulin deficiency in the brain activates an insulin signaling pathway that may promote neurodegeneration
T2 - iScience
J2 - iScience
PY - 2026
DA - 2026/
VL - 29
IS - 5
SP - 115720
SN - 2589-0042
PB - Elsevier
DO - 10.1016/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1016/
"type": "article-journal",
"title": "Progranulin deficiency in the brain activates an insulin signaling pathway that may promote neurodegeneration",
"container-title": "iScience",
"author": [
{
"family": "Sajan",
"given": "Mini P."
},
{
"family": "Aggarwal",
"given": "Geetika"
},
{
"family": "Hwang",
"given": "Joel Jihwan"
},
{
"family": "Smith",
"given": "Denise M."
},
{
"family": "Cooper",
"given": "Denise R."
},
{
"family": "Duncan",
"given": "Mildred Acevedo"
},
{
"family": "Hansen",
"given": "Barbara C."
},
{
"family": "Nguyen",
"given": "Andrew D."
},
{
"family": "Farese",
"given": "Robert V."
}
],
"container-title-short":
"volume": "29",
"issue": "5",
"page": "115720",
"DOI": "10.1016/
"PMID": "42095076",
"PMCID": "PMC13141651",
"ISSN": "2589-0042",
"publisher": "Elsevier",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
12
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1016/j.nbd.2026.107475
- Human TDP-43 expression worsens FTD-related phenotypes in progranulin-insufficient
mice. Journal: Neurobiology of diseaseIn common: cellular / molecular, 11 references - [2] doi:10.1172/jci190035 [code]
- TGF-β signaling promotes astroglial activation and TDP-43 proteinopathy in organoid models of frontotemporal lobar degeneration.Journal: The Journal of clinical investigationIn common: cellular / molecular, 2 references
- [3] doi:10.1007/s11033-026-11965-x [code]
- Biological pathways related to mirna-125a-5p in behavioral variant of frontotemporal dementia.Journal: Molecular biology reportsIn common: cellular / molecular, 2 references
- [4] doi:10.1038/s41588-026-02570-6 [code]
- Somatic mosaicism in ALS and FTD identifies focal mutations associated with widespread degeneration.Journal: Nature geneticsIn common: cellular / molecular, 2 references
- [5] doi:10.1007/s43440-026-00866-2
- Selective non-nuclear estrogen receptor activation with PaPE-1 evokes neuroprotection involving mTOR/
MEK in an in vitro model of hypoxic/ ischemic injury. Journal: Pharmacological reports : PRIn common: cellular / molecular, 1 reference - [6] doi:10.1186/s12964-026-02748-9
- Neuroinflammation-induce
d downregulation of RAB7 in murine astrocytes disrupts endo-lysosomal homeostasis and induces astrogliosis. Journal: Cell communication and signaling : CCSIn common: cellular / molecular, 1 reference - [7] doi:10.3390/ijms27177542
- Assessment of the Association of Periodontitis and Diabetes Mellitus with Alzheimer's Disease in a Mouse Model.Journal: International journal of molecular sciencesIn common: cellular / molecular, 1 reference
- [8] doi:10.1007/s12035-026-06014-4
- Hypothalamus Amyloid Levels Are Associated with Early Sex-Dependent Alterations in Peripheral Energy Homeostasis in TgF344-AD Rats.Journal: Molecular neurobiologyIn common: cellular / molecular, 1 reference
- [9] doi:10.1186/s12987-026-00825-2
- Acute amyloid-β exposure disrupts insulin signaling in hCMEC/
D3 blood-brain barrier endothelial cells. Journal: Fluids and barriers of the CNSIn common: cellular / molecular, 1 reference - [10] doi:10.1126/sciadv.aeb7558
- An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling.Journal: Science advancesIn common: cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.