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Record W4406223002 · doi:10.1002/alz.095074

A novel culprit in glucose hypometabolism in Alzheimer’s disease

2024· article· en· W4406223002 on OpenAlexaff
Ylauna Christine Mégane Penalva, Jessica Cinkornpumin, Mari T. Kaartinen, William A. Pastor, Lisa Marie Munter

Bibliographic record

VenueAlzheimer s & Dementia · 2024
Typearticle
Languageen
FieldMedicine
TopicNatural Antidiabetic Agents Studies
Canadian institutionsMcGill University
Fundersnot available
KeywordsCulpritDiseaseMedicineDiabetes mellitusCardiologyInternal medicineEndocrinologyMyocardial infarction

Abstract

fetched live from OpenAlex

Abstract Background Alzheimer’s disease is characterized by early decreases in cerebral glucose metabolism which are linked to reduced glucose transporter 1 (GLUT1) expression at the blood‐brain barrier (BBB). Another key disease hallmark is the abundance of Aβ peptides as plaques in the brain which arise from the processing of the amyloid precursor protein (APP). Autosomal dominant inherited mutations causatively link APP itself to AD, rendering it imperative to fully understand APP’s physiological functions to define the underlying biology of AD. Previous studies in APP knockout (KO) mice implicate APP in metabolic processes such as mitochondrial function and insulin action. However, GLUT1 regulation as well as glucose metabolism at the BBB has yet to be investigated. Method We use APP KO mouse embryonic fibroblasts (MEFs), mouse primary cerebral endothelial cells, and vessels enriched from mouse brains to study GLUT1 physiology. RNAseq data was collected in MEFs to determine transcriptional changes underlying studied phenotypes. Result Seahorse analysis of APP KO MEFs revealed a 50% decrease in glycolytic activity and 75% decrease in mitochondrial respiration as compared to control. Glucose uptake was also significantly decreased in the absence of APP. These metabolic defects were underlined by a 2‐fold decrease in GLUT1 total expression and a 5‐fold decrease in GLUT1 cell surface levels. The investigation of signaling pathways responsible for GLUT1 upregulation showed that PI3K/Akt/mTORC pathway was downregulated in APP KO MEFs as compared to control. Primary cerebral endothelial cells and vessels recapitulated the decrease in GLUT1 expression as well as decreased activation of the PI3K/Akt/mTORC pathway, suggesting a completely novel role for APP in cerebral glucose metabolism. Analysis of RNAseq data collected in MEFs for pathways regulating glucose metabolism revealed widespread changes in extracellular matrix gene expression. Conclusion Our findings posit APP as a major regulator of GLUT1 expression and glucose metabolism. This new perspective on APP is crucial for AD therapy as novel approaches could be developed to target decreased cerebral glucose metabolism.

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 distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: none
Teacher disagreement score0.779
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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 head0.035
GPT teacher head0.298
Teacher spread0.263 · 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 teacher head, not a consensus.

Study designObservational
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
Published2024
Admission routes1
Has abstractyes

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