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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with a complex etiology. While emerging AD therapeutics can slow cognitive decline, they may worsen dementia in certain groups of individuals. Therefore, alternative treatments are much needed. Microglia, the brain resident macrophages, have the potential to be novel therapeutic targets as they regulate many facets of AD, including lipid droplet (LD) accumulation, amyloid beta (Aβ) clearance, and neuroinflammation. To carry out such functions, microglia undergo phenotypic changes, which are linked to shifts in metabolism and substrate utilization. While homeostatic microglia are driven by oxidative phosphorylation (OXPHOS) and glycolysis, in aging and AD, microglia shift further towards glycolysis. Interestingly, this "metabolic reprogramming" may be linked to an increase in fructose metabolism. In the brain, microglia predominantly express the fructose transporter SLC2A5 (GLUT5), and enzymes involved in fructolysis and endogenous fructose production, with their expression being upregulated in aging and disease. Here, we review evidence for fructose uptake, breakdown, and production in microglia. We also evaluate emerging literature targeting fructose metabolism in the brain and periphery to assess its ability to modulate microglial function in AD. The ability of microglia to transport and utilize fructose, coupled with the well-established role of fructose in metabolic dysfunction, supports the notion that microglial fructose metabolism may be a novel potential therapeutic target for AD.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Sturno, A. M., Hassell, J. E., Lanaspa, M. A., & Bruce, K. D. (2025). Do microglia metabolize fructose in Alzheimer’s disease? Journal of Neuroinflammation. https://doi.org/10.1186/s12974-025-03401-x

Vancouver

Sturno AM, Hassell JE, Lanaspa MA, Bruce KD. Do microglia metabolize fructose in Alzheimer’s disease? Journal of Neuroinflammation. 2025. doi:10.1186/s12974-025-03401-x. PMID: 40089786.

BibTeX

@article{sturno2025-40089786,
  author  = {Sturno, Annalise M. and Hassell, James E. and Lanaspa, Miguel Angel and Bruce, Kimberley D.},
  title   = {{Do microglia metabolize fructose in Alzheimer’s disease?}},
  journal = {Journal of Neuroinflammation},
  year    = {2025},
  doi     = {10.1186/s12974-025-03401-x},
  pmid    = {40089786},
  url     = {https://doi.org/10.1186/s12974-025-03401-x}
}

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Key findings

Interestingly, this "metabolic reprogramming" may be linked to an increase in fructose metabolism.
In the brain, microglia predominantly express the fructose transporter SLC2A5 (GLUT5), and enzymes involved in fructolysis and endogenous fructose production, with their expression being upregulated in aging and disease.
Here, we review evidence for fructose uptake, breakdown, and production in microglia.
We also evaluate emerging literature targeting fructose metabolism in the brain and periphery to assess its ability to modulate microglial function in AD.
The ability of microglia to transport and utilize fructose, coupled with the well-established role of fructose in metabolic dysfunction, supports the notion that microglial fructose metabolism may be a novel potential therapeutic target for AD.

Why it matters

This review examines evidence that microglia take up, break down, and produce fructose and that this may be linked to metabolic changes in aging and Alzheimer's disease. It evaluates targeting fructose metabolism as a way to modulate microglial function but does not show a treatment.

Study details

Evidence strengthLow

How this study scored 41/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of Neuroinflammation)
Journal's citation record	2 / 4	Journal of Neuroinflammation: journal h-index 216 (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	2025 — 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)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	3 / 7	Cited 17 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	5.7 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 5.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	2 / 4	Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Kimberley D. Bruce: h-index 27 (OpenAlex, whole career)
Institution's track record	1 / 3	University of Colorado Anschutz: institution h-index 768 (OpenAlex)
Multi-centre collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 40089786)
Free to read	2 / 2	Free to read
Total	41 / 100	—

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