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61/100

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %). Brain glucose hypometabolism determined pathway selection with significant effects: participants with severe hypometabolism (FDG z-score < -0.5) demonstrated 7.4-fold acceleration in direct conversion velocity compared to preserved metabolism (17.12 vs 2.31 per 100 person-years, P-value<0.001). Pathway prediction models achieved excellent discrimination for direct conversion (AUC = 0.994) and acceptable performance for sequential pathways (AUC = 0.680). Metabolic phenotyping demonstrated peculiar vulnerability profiles, cognitive stability maintained metabolic reserve (FDG +0.57 ± 0.58), while rapid converters demonstrated metabolic failure patterns (FDG -0.18 ± 0.88). Based on our modeling findings, we observed that brain glucose metabolism could serve as a pathway determinant rather than simply a decline predictor, which could play a promising role in precision medicine approaches to Alzheimer's disease prevention. FDG-PET biomarkers can stratify individuals for pathway-specific interventions, transforming reactive dementia care into proactive pathway-guided management.

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

APA 7th

Alhasan, M. S., Alhasan, A. S., Milburn, J. M., Khalil, M., Almaghraby, A., Alharthi, O. A., et al. (2025). FDG-PET brain glucose hypometabolism predicts Alzheimer's disease progression pathways in cognitively normal adults: A longitudinal competing risks modeling. Metabolism Open. https://doi.org/10.1016/j.metop.2025.100400

Vancouver

Alhasan MS, Alhasan AS, Milburn JM, Khalil M, Almaghraby A, Alharthi OA, et al. FDG-PET brain glucose hypometabolism predicts Alzheimer's disease progression pathways in cognitively normal adults: A longitudinal competing risks modeling. Metabolism Open. 2025. doi:10.1016/j.metop.2025.100400. PMID: 41089337.

BibTeX

@article{alhasan2025-41089337,
  author  = {Alhasan, Mustafa S. and Alhasan, Ayman S. and Milburn, James Michael and Khalil, Mohammed and Almaghraby, Abdullah and Alharthi, Omar A. and Hamoud, Seham and Essibayi, Muhammed Amir and others},
  title   = {{FDG-PET brain glucose hypometabolism predicts Alzheimer's disease progression pathways in cognitively normal adults: A longitudinal competing risks modeling}},
  journal = {Metabolism Open},
  year    = {2025},
  doi     = {10.1016/j.metop.2025.100400},
  pmid    = {41089337},
  url     = {https://doi.org/10.1016/j.metop.2025.100400}
}

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How to read this study

Design: this is a follow-up (cohort) study. People are observed over time and not assigned to anything, so an association can reflect other differences between groups. Look at how long follow-up lasted, how many dropped out, and whether the authors adjusted for age, education and other health conditions.
Size: the record lists 1,136 participants. Ask whether that is enough for the question, and who they were.
Effect: the record reports “AUC = 0.994; AUC = 0.680”. A statistically significant result can still be small in daily life.

What the evidence grade means here

This page is graded moderate. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Moderate means the abstract mentions a cohort, case-control or longitudinal design. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %).
Brain glucose hypometabolism determined pathway selection with significant effects: participants with severe hypometabolism (FDG z-score < -0.5) demonstrated 7.4-fold acceleration in direct conversion velocity compared to preserved metabolism (17.12 vs 2.31 per 100 person-years, P-value<0.001).
Pathway prediction models achieved excellent discrimination for direct conversion (AUC = 0.994) and acceptable performance for sequential pathways (AUC = 0.680).
Metabolic phenotyping demonstrated peculiar vulnerability profiles, cognitive stability maintained metabolic reserve (FDG +0.57 ± 0.58), while rapid converters demonstrated metabolic failure patterns (FDG -0.18 ± 0.88).
Based on our modeling findings, we observed that brain glucose metabolism could serve as a pathway determinant rather than simply a decline predictor, which could play a promising role in precision medicine approaches to Alzheimer's disease prevention.

Why it matters

This longitudinal modeling study found four progression pathways and showed that severe brain glucose hypometabolism on FDG-PET was linked to a 7.4-fold faster direct conversion to dementia compared with preserved metabolism. It does not test a treatment or cure, but it suggests FDG-PET may help stratify people for pathway-specific prevention approaches.

Study details

Study designlongitudinal study
Participants1,136
Effect sizeAUC = 0.994; AUC = 0.680
Evidence strengthModerate

How this study scored 61/100

Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Metabolism Open)
Journal's citation record	0 / 4	Metabolism Open: journal h-index 37 (OpenAlex, 2026-10-29)
Study design	7 / 12	A longitudinal study following the same people over time
Strength of evidence	3 / 5	Rated “moderate” 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	3 / 4	1,136 participants
Effect reported	3 / 3	Effect reported with a statistic (interval, p-value, ratio or similar)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	2 / 7	Cited 11 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	3.7 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 7.0× 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	1 / 4	Cited 11 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Ahmed Y. Azzam: h-index 58 (OpenAlex, whole career)
Institution's track record	2 / 3	The University of Queensland: institution h-index 1,516 (OpenAlex)
Multicenter collaboration	3 / 3	OpenAlex lists 10 institution(s) in 4 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41089337)
Free to read	2 / 2	Free to read
Total	61 / 100	—

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