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Record W7117100694 · doi:10.1002/alz70855_105337

Examining the Role of <i>SORL1</i> in Driving Alzheimer's Disease‐Related Alterations in Endolysosomal Trafficking in Neurons and Microglia

2025· article· en· W7117100694 on OpenAlexaff
Brooke A. DeRosa, Yalun Zhang, C. Golightly, Lauren Coombs, Lauren E. Rothschild, Brian W Kunkle, Michael Cuccaro, Jeffery M. M Vance, Margaret Pericak‐Vance, Peter St George‐Hyslop, Derek M. Dykxhoorn

Bibliographic record

VenueAlzheimer s & Dementia · 2025
Typearticle
Languageen
FieldMedicine
TopicAlzheimer's disease research and treatments
Canadian institutionsUniversity of Toronto
Fundersnot available
KeywordsMicrogliaPhenotypeEndocytosisCell typeNeuronEndosomeCell

Abstract

fetched live from OpenAlex

Abstract Background Disruption of endolysosomal trafficking is a key pathogenic driver in Alzheimer's disease (AD). Among the genes linked to the endosomal pathway in AD, SORL1 is recognized as one of the most significant risk factors. SORL1 encodes an endocytic sorting receptor that regulates endosomal trafficking and processing of crucial AD‐related molecules, including pathogenic forms of amyloid‐β (e.g., Aβ42) and amyloid precursor protein (APP). Using complementary cell‐based models, we examined the impact of a protein‐truncating variant of SORL1 on endolysosomal trafficking and APP processing. Method Induced pluripotent stem cell (iPSC) lines were generated from two siblings with early‐onset AD carrying a rare protein‐truncating deletion in SORL1 (rs1343336951; p.C1431fs). SORL1 wild‐type isogenic control iPSC lines were created using CRISPR/Cas9 from these patient‐derived lines. Following validation, the iPSCs were differentiated into forebrain neurons and microglia to assess the impact of the SORL1 deletion on endolysosomal trafficking in each cell‐type. Additional analyses were performed in HEK293‐APPswe cells overexpressing either wild‐type SORL1 or the C1431fs variant. Result In HEK293‐APPswe cells, the C1431fs variant enhanced secretion of Aβ42 ( p <0.01), Aβ40 ( p <0.01), as well as soluble α‐secretase (sAPPα; p <0.01) and β‐secretase (sAPPβ; p <0.01) cleavage products. Furthermore, C1431fs led to an increase in the secretion of soluble SORL1 ( p <0.01). Surface biotinylation experiments showed that C1431fs reduced levels of SORL1 at the cell surface ( p <0.05), while increasing the surface levels of APP ( p <0.05). In SORL1 +/C1431fs neurons, we observe an accumulation of APP in early endosomes ( p = 0.002), endosomal swelling ( p = 0.004), and a higher number of early endosomes per cell ( p = 0.018). Additionally, SORL1 +/C1431fs neurons trend toward increased secretion of Aβ42 compared to controls. Our analysis of phagocytosis in SORL1 +/C1431fs microglia, assessed by the uptake of pHrodo‐labeled fibrillar Aβ42, suggests that the deletion reduces phagocytic activity. Current investigations in microglia are evaluating the concentration of specific cytokines and chemokines secreted in response to proinflammatory stimuli. Conclusion Our findings suggest that the SORL1 C1431fs deletion is capable of inducing defects in endolysosomal trafficking in both neurons and microglia. Ongoing studies in SORL1 +/C1431fs microglia and neurons will further expand our understanding of SORL1's role in regulating endolysosomal phenotypes across multiple cell types implicated in AD.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.020
GPT teacher head0.280
Teacher spread0.261 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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