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Glucose metabolism in normal aging and Alzheimer's disease: Methodological and physiological considerations for PET studies
Mosconi L.. Clinical and translational imaging, 2013-08-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder associated with progressive loss of cognitive function. 2-[ 18 F]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) has long been used to measure resting-state cerebral metabolic rates of glucose, a proxy for neuronal activity. Several FDG PET studies have shown that metabolic reductions occur decades before onset of AD symptoms, suggesting that metabolic deficits may be an upstream event in at least some late-onset AD cases. This review explores this possibility, initially discussing the link between AD pathology, neurodegeneration, oxidative stress and AD, and then discussing findings of FDG PET hypometabolism in AD patients as well as in at-risk individuals, especially those with a first-degree family history of late-onset AD. While the rare early-onset form of AD is due to autosomal dominant genetic mutations, the etiology and pathophysiology of age-dependent, late-onset AD is more complex. Recent FDG PET studies have shown that adult children of AD-affected mothers are more likely than those with AD-fathers to show AD-like brain changes. Given the connection between glucose metabolism and mitochondria, and the fact that mitochondrial DNA is maternally inherited in humans, it is here argued that altered bioenergetics may be an upstream event in those with a maternal history of late-onset AD. Biomarkers of AD have great potential for identifying AD endophenotypes in at-risk individuals, which may help direct investigation of potential susceptibility genes.
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APA 7th
Mosconi, L. (2013). Glucose metabolism in normal aging and Alzheimer's disease: Methodological and physiological considerations for PET studies. Clinical and translational imaging. https://doi.org/10.1007/s40336-013-0026-y
Vancouver
Mosconi L. Glucose metabolism in normal aging and Alzheimer's disease: Methodological and physiological considerations for PET studies. Clinical and translational imaging. 2013. doi:10.1007/s40336-013-0026-y. PMID: 24409422.
BibTeX
@article{mosconi2013-24409422,
author = {Mosconi, L.},
title = {{Glucose metabolism in normal aging and Alzheimer's disease: Methodological and physiological considerations for PET studies}},
journal = {Clinical and translational imaging},
year = {2013},
doi = {10.1007/s40336-013-0026-y},
pmid = {24409422},
url = {https://doi.org/10.1007/s40336-013-0026-y}
}
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Key findings
- Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder associated with progressive loss of cognitive function. 2-[ 18 F]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) has long been used to measure resting-state cerebral metabolic rates of glucose, a proxy for neuronal activity.
- Several FDG PET studies have shown that metabolic reductions occur decades before onset of AD symptoms, suggesting that metabolic deficits may be an upstream event in at least some late-onset AD cases.
- Recent FDG PET studies have shown that adult children of AD-affected mothers are more likely than those with AD-fathers to show AD-like brain changes.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Clinical and translational imaging) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2013 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24409422) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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