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Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease
Mosconi L, Pupi A, De Leon MJ.. Annals of the New York Academy of Sciences, 2008-12-01
Topic: Amyloid, tau and blood-test diagnosis
One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc). In vivo imaging using positron emission tomography with 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG-PET) demonstrates consistent and progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. Increasing evidence suggests that CMRglc reductions occur at the preclinical stages of AD. CMRglc reductions were observed on FDG-PET before the onset of disease in several groups of at-risk individuals, including patients with mild cognitive impairment (MCI), often a prodrome to AD; presymptomatic individuals carrying mutations responsible for early-onset familial AD; cognitively normal elderly individuals followed for several years until they declined to MCI and eventually to AD; normal, middle-aged individuals who expressed subjective memory complaints and were carriers of the apolipoprotein E epsilon-4 allele, a strong genetic risk factor for late-onset AD. However, the causes of the early metabolic dysfunction forerunning the onset of AD are not known. An increasing body of evidence indicates a deficient or altered energy metabolism that could change the overall oxidative microenvironment for neurons during the pathogenesis and progression of AD, leading to alterations in mitochondrial enzymes and in glucose metabolism in AD brain tissue. The present paper reviews findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mosconi, L., Pupi, A., & De Leon, M. J. (2008). Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease. Annals of the New York Academy of Sciences. https://doi.org/10.1196/annals.1427.007
Vancouver
Mosconi L, Pupi A, De Leon MJ. Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease. Annals of the New York Academy of Sciences. 2008. doi:10.1196/annals.1427.007. PMID: 19076441.
BibTeX
@article{mosconi2008-19076441,
author = {Mosconi, L. and Pupi, A. and De Leon, M. J.},
title = {{Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease}},
journal = {Annals of the New York Academy of Sciences},
year = {2008},
doi = {10.1196/annals.1427.007},
pmid = {19076441},
url = {https://doi.org/10.1196/annals.1427.007}
}
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Key findings
- Increasing evidence suggests that CMRglc reductions occur at the preclinical stages of AD.
- An increasing body of evidence indicates a deficient or altered energy metabolism that could change the overall oxidative microenvironment for neurons during the pathogenesis and progression of AD, leading to alterations in mitochondrial enzymes and in glucose metabolism in AD brain tissue.
Why it matters
This review describes evidence that reduced cerebral glucose metabolism occurs at preclinical stages of Alzheimer's disease in at-risk groups, and links this to altered energy metabolism and oxidative stress. It reports no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 51/100
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 (Annals of the New York Academy of Sciences) |
| Journal's citation record | 3 / 4 | Annals of the New York Academy of Sciences: journal h-index 399 (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 | 1 / 5 | 2008 — within 20 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 | 6 / 7 | Cited 596 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 29.8 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 4 / 6 | Cited 13.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 15 other studies in this library |
| Still being cited | 3 / 4 | Cited 111 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Mony J. de Leon: h-index 127 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | New York University: institution h-index 1,612 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19076441) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
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