Composite
46%
Novelty
50%
Feasibility
30%
Impact
55%
Mechanistic
55%
Druggability
40%
Safety
35%
Confidence
55%

Mechanistic description

Restoration of Neuronal Ketone Body Utilization via MCT1 Upregulation

Mechanism / pathway

  1. SLC16A1 (MCT1)
  2. metabolomics

Evidence for (4)

  • Human AD prefrontal cortex shows 40-60% reduction in MCT1 and MCT4 protein expression compared to age-matched controls

  • Ketogenic diet intervention in MCI patients improves cognitive outcomes and increases serum ketone bodies

  • Mouse model of AD (APP/PS1) demonstrates that ketone supplementation improves mitochondrial function only when MCT expression is preserved

  • CSF β-hydroxybutyrate levels correlate inversely with dementia severity

Evidence against (4)

  • Ketogenic diets show limited CNS ketone uptake in humans - using 11C-acetoacetate PET, ketones enter brain but uptake saturates at physiological levels

  • Clinical trials of ketone esters in AD show modest brain uptake - cerebral metabolic improvement is limited

  • MCT1 has bidirectional transport function - upregulation could increase lactate efflux from neurons, potentially worsening energy balance

  • APP/PS1 mouse models may not recapitulate human AD ketone metabolism - species differences in MCT expression patterns are significant

Evidence matrix

4 supporting 4 contradicting
60% posterior support

Supporting

  • Human AD prefrontal cortex shows 40-60% reduction in MCT1 and MCT4 protein expression compared to age-matched controls PMID:25716827
  • Ketogenic diet intervention in MCI patients improves cognitive outcomes and increases serum ketone bodies PMID:29108873
  • Mouse model of AD (APP/PS1) demonstrates that ketone supplementation improves mitochondrial function only when MCT expression is preserved PMID:30355646
  • CSF β-hydroxybutyrate levels correlate inversely with dementia severity PMID:31978580

Contradicting

  • Ketogenic diets show limited CNS ketone uptake in humans - using 11C-acetoacetate PET, ketones enter brain but uptake saturates at physiological levels PMID:28642376
  • Clinical trials of ketone esters in AD show modest brain uptake - cerebral metabolic improvement is limited PMID:31170379
  • MCT1 has bidirectional transport function - upregulation could increase lactate efflux from neurons, potentially worsening energy balance PMID:25411495
  • APP/PS1 mouse models may not recapitulate human AD ketone metabolism - species differences in MCT expression patterns are significant PMID:30059790

Bayesian persona consensus

60% posterior support

4 signals · 3 for / 1 against · agreement 75%

scidex.consensus.bayesian compounds vote / rank / fund signals from 4 contributing personas in log-odds space, weighted by uniform. Prior 50%.

Cite this hypothesis

Cite this hypothesis
Citation

etl-backfill (2026). Restoration of Neuronal Ketone Body Utilization via MCT1 Upregulation. SciDEX hypothesis. https://prism.scidex.ai/hypotheses/h-40d0524f

BibTeX
@misc{scidex_hypothesis_h40d0524,
  title        = {Restoration of Neuronal Ketone Body Utilization via MCT1 Upregulation},
  author       = {etl-backfill},
  year         = {2026},
  howpublished = {SciDEX hypothesis},
  url          = {https://prism.scidex.ai/hypotheses/h-40d0524f},
  note         = {SciDEX artifact hypothesis:h-40d0524f}
}

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POST /api/scidex/rpc
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    "content_type": "hypothesis",
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