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The use of PET in Alzheimer disease
Nordberg A, Rinne JO, Kadir A, Långström B.. Nature reviews. Neurology, 2010-02-01
Topic: Amyloid, tau and blood-test diagnosis
In Alzheimer disease (AD), which is the most common cause of dementia, the underlying disease pathology most probably precedes the onset of cognitive symptoms by many years. Thus, efforts are underway to find early diagnostic markers as well as disease-modifying treatments for this disorder. PET enables various brain systems to be monitored in living individuals. In patients with AD, PET can be used to investigate changes in cerebral glucose metabolism, various neurotransmitter systems, neuroinflammation, and the protein aggregates that are characteristic of the disease, notably the amyloid deposits. These investigations are helping to further our understanding of the complex pathophysiological mechanisms that underlie AD, as well as aiding the early and differential diagnosis of the disease in the clinic. In the future, PET studies will also be useful for identifying new therapeutic targets and monitoring treatment outcomes. Amyloid imaging could be useful as early diagnostic marker of AD and for selecting patients for anti-amyloid-beta therapy, while cerebral glucose metabolism could be a suitable PET marker for monitoring disease progression. For the near future, multitracer PET studies are unlikely to be used routinely in the clinic for AD, being both burdensome and expensive; however, such studies are very informative in a research context.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Nordberg, A., Rinne, J. O., Kadir, A., & Långström, B. (2010). The use of PET in Alzheimer disease. Nature reviews. Neurology. https://doi.org/10.1038/nrneurol.2009.217
Vancouver
Nordberg A, Rinne JO, Kadir A, Långström B. The use of PET in Alzheimer disease. Nature reviews. Neurology. 2010. doi:10.1038/nrneurol.2009.217. PMID: 20139997.
BibTeX
@article{nordberg2010-20139997,
author = {Nordberg, A. and Rinne, J. O. and Kadir, A. and Långström, B.},
title = {{The use of PET in Alzheimer disease}},
journal = {Nature reviews. Neurology},
year = {2010},
doi = {10.1038/nrneurol.2009.217},
pmid = {20139997},
url = {https://doi.org/10.1038/nrneurol.2009.217}
}
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Key findings
- In patients with AD, PET can be used to investigate changes in cerebral glucose metabolism, various neurotransmitter systems, neuroinflammation, and the protein aggregates that are characteristic of the disease, notably the amyloid deposits.
- These investigations are helping to further our understanding of the complex pathophysiological mechanisms that underlie AD, as well as aiding the early and differential diagnosis of the disease in the clinic.
- In the future, PET studies will also be useful for identifying new therapeutic targets and monitoring treatment outcomes.
- Amyloid imaging could be useful as early diagnostic marker of AD and for selecting patients for anti-amyloid-beta therapy, while cerebral glucose metabolism could be a suitable PET marker for monitoring disease progression.
- For the near future, multitracer PET studies are unlikely to be used routinely in the clinic for AD, being both burdensome and expensive; however, such studies are very informative in a research context.
Why it matters
This 2010 review describes how PET brain scans can show glucose use, brain chemical systems, inflammation and amyloid deposits in living people with Alzheimer's, and says such scans are aiding early and differential diagnosis. It suggests amyloid imaging "could be useful as early diagnostic marker" and for choosing patients for anti-amyloid therapy, while glucose PET "could be a suitable" marker for tracking progression. It reports no new data, and the authors say multi-tracer PET is too burdensome and expensive to become routine clinical care soon.
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Study details
- Evidence strengthLow
How this study scored 49/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature reviews. Neurology) |
| Journal's citation record | 3 / 4 | Nature Reviews Neurology: journal h-index 269 (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 | 2010 — 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 | 6 / 7 | Cited 452 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 25.1 citations a year over 18 year(s) since 2010 |
| Impact for its field and year | 3 / 6 | Cited 5.1× 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 68 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Bengt Långström: h-index 86 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Karolinska Institutet: institution h-index 1,477 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20139997) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
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