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Record W4406030166 · doi:10.1002/alz.092619

Investigating the role of <i>SORL1</i> in mediating AD‐specific endolysosomal phenotypes in neurons and microglia

2024· article· en· W4406030166 on OpenAlexaff
Brooke A. DeRosa, Yalun Zhang, C. Golightly, Lauren Coombs, Lauren E. Rothschild, Brian W. Kunkle, Michael L. Cuccaro, Jeffery M. Vance, Margaret A Pericak‐Vance, Peter St George‐Hyslop, Derek M. Dykxhoorn

Bibliographic record

VenueAlzheimer s & Dementia · 2024
Typearticle
Languageen
FieldMedicine
TopicAlzheimer's disease research and treatments
Canadian institutionsUniversity of Toronto
Fundersnot available
KeywordsEndosomeBiologyMicrogliaAmyloid precursor proteinCell biologyEndocytic cycleHEK 293 cellsPhenotypeSecretionAlzheimer's diseaseCell cultureCellImmunologyGeneticsGeneEndocytosisInflammationInternal medicineBiochemistryMedicineDiseaseIntracellular

Abstract

fetched live from OpenAlex

Abstract Background Dysregulation of endolysosomal trafficking is a major pathogenic mechanism in Alzheimer’s disease (AD). From the family of AD‐linked endosomal pathway genes, SORL1 stands out as one of the highest risk factors. SORL1 encodes an endocytic sorting receptor that mediates endosomal trafficking and processing of key AD‐associated molecules, including pathogenic forms of amyloid‐β (e.g., Aβ42) and amyloid precursor protein (APP). Using complementary cell‐based model systems, we investigated the role of a protein‐truncating SORL1 variant on endolysosomal trafficking and APP processing. Method Induced pluripotent stem cell (iPSC) lines were derived from two siblings affected with early onset AD (EOAD) who carried a rare protein‐truncating deletion in SORL1 (rs1343336951; p.C1431fs). SORL1+/+ isogenic control iPSC lines were created from the patient lines using CRISPR/Cas9. After validation, the iPSC lines were differentiated into forebrain neurons and analyzed for endosomal trafficking defects. Additional analyses were completed in HEK293‐APPswe cells overexpressing SORL1 wild‐type (WT) or the C1431fs variant. Studies are underway that examine SORL1+/C1431fs microglia for defects in endolysosomal function. Result SORL1+/C1431fs neurons have increased localization of APP in early endosomes (p = 0.002), endosomal swelling (p = 0.004), and greater numbers of early endosomes per cell (p = 0.018). We additionally observe SORL1+/C1431fs neurons trending toward increased secretion of Aβ42 compared to controls. In HEK293 cells, C1431fs increased secretion of Aβ42 (p < 0.01), Aβ40 (p < 0.01), as well as APP soluble α‐secretase (sAPPα; p < 0.01) and β‐secretase (sAPPβ; p < 0.01) cleavage products. We additionally found C1431fs led to increased secretion of soluble SORL1 (p < 0.01). Surface biotinylation revealed C1431fs led to lower levels of SORL1 detected at the cell surface (p < 0.05). Conversely, C1431fs increased the amount of surface APP (p < 0.05). Conclusion Our results indicate that a single gene copy of the SORL1 C1431fs variant is sufficient to induce neuronal defects in endosomal trafficking and APP processing. Our findings are consistent with previously reported results from similar studies of SORL1 in cultured neurons. Ongoing studies in SORL1+/C1431fs microglia and neurons will help broaden our understanding of the role SORL1 plays in regulating endolysosomal phenotypes in 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 score0.005

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 integrity0.0000.001
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 head0.023
GPT teacher head0.280
Teacher spread0.256 · 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

Citations1
Published2024
Admission routes1
Has abstractyes

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