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Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies
Minhas PS, Jones JR, Latif-Hernandez A, Sugiura Y, Durairaj AS, Wang Q, Mhatre SD, Uenaka T et al.. Science (New York, N.Y.), 2024-08-23
Topic: Amyloid, tau and blood-test diagnosis
Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD. We report that inhibition of indoleamine-2,3-dioxygenase 1 (IDO1), which metabolizes tryptophan to kynurenine (KYN), rescues hippocampal memory function in mouse preclinical models of AD by restoring astrocyte metabolism. Activation of astrocytic IDO1 by amyloid β and tau oligomers increases KYN and suppresses glycolysis in an aryl hydrocarbon receptor-dependent manner.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Minhas, P. S., Jones, JR., Latif-Hernandez, A., Sugiura, Y., Durairaj, A. S., Wang, Q., et al. (2024). Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies. Science (New York, N.Y.). https://doi.org/10.1126/science.abm6131
Vancouver
Minhas PS, Jones JR, Latif-Hernandez A, Sugiura Y, Durairaj AS, Wang Q, et al. Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies. Science (New York, N.Y.). 2024. doi:10.1126/science.abm6131. PMID: 39172838.
BibTeX
@article{minhas2024-39172838,
author = {Minhas, P. S. and Jones, JR. and Latif-Hernandez, A. and Sugiura, Y. and Durairaj, A. S. and Wang, Q. and Mhatre, S. D. and Uenaka, T. and others},
title = {{Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies}},
journal = {Science (New York, N.Y.)},
year = {2024},
doi = {10.1126/science.abm6131},
pmid = {39172838},
url = {https://doi.org/10.1126/science.abm6131}
}
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Key findings
- We report that inhibition of indoleamine-2,3-dioxygenase 1 (IDO1), which metabolizes tryptophan to kynurenine (KYN), rescues hippocampal memory function in mouse preclinical models of AD by restoring astrocyte metabolism.
- Activation of astrocytic IDO1 by amyloid β and tau oligomers increases KYN and suppresses glycolysis in an aryl hydrocarbon receptor-dependent manner.
- In amyloid and tau models, IDO1 inhibition improves hippocampal glucose metabolism and rescues hippocampal long-term potentiation in a monocarboxylate transporter-dependent manner.
- In astrocytic and neuronal cocultures from AD subjects, IDO1 inhibition improved astrocytic production of lactate and uptake by neurons.
Why it matters
In mouse models of Alzheimer's disease, inhibiting indoleamine-2,3-dioxygenase 1 restored astrocyte metabolism, improved hippocampal glucose metabolism and rescued hippocampal memory function. This is preclinical animal work, so it does not yet show a treatment or cure for Alzheimer's disease in people.
Study details
- Evidence strengthLow
How this study scored 61/100
Published in a top-tier journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 10 / 10 | Tier 1 — top-tier general journal (Science (New York, N.Y.)) |
| Journal's citation record | 4 / 4 | Science: journal h-index 1,754 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2024 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 230 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 57.5 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 6 / 6 | Cited 54.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 4 / 4 | Cited 229 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Katrin I. Andreasson: h-index 53 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Stanford University: institution h-index 2,684 (OpenAlex) |
| Multicenter collaboration | 3 / 3 | OpenAlex lists 10 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39172838) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 61 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1126/science.abm6131
- PubMed: 39172838
- Original source →
- Free full text: Europe PMC (PubMed Central) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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