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Amyloid PET Ligands for Dementia
Villemagne VL, Rowe CC.. PET clinics, 2010-01-01
Topic: Amyloid, tau and blood-test diagnosis
The progressive nature of neurodegeneration suggests an age-dependent process that ultimately leads to synaptic failure and neuronal damage in cortical areas of the brain critical for memory and higher mental functions. The increasing age of the population in developed countries suggests that, if unchecked, these disorders will become increasingly prevalent. In the absence of specific biologic markers, direct pathologic examination of brain tissue still is the only definitive method for establishing a diagnosis of Alzheimer disease (AD) and other types of dementia. Pathologic hallmarks of AD are intracellular neurofibrillary tangles (NFT) and extracellular amyloid plaques. NFT are intraneuronal bundles of paired helical filaments mainly composed of the aggregates of an abnormally phosphorylated form of tau protein; neuritic plaques consist of dense extracellular aggregates of β-amyloid (Aβ), surrounded by reactive gliosis and dystrophic neurites. To date, all available evidence strongly supports the notion that an imbalance between the production and removal of Aβ leading to its progressive accumulation is central to the pathogenesis of AD. A growing understanding of the molecular mechanisms of Aβ formation, degradation, and neurotoxicity is being translated into new therapeutic approaches. Whereas AD is the most common cause of dementia in the elderly, postmortem studies have found dementia with Lewy Bodies and frontotemporal lobe degeneration each to account for about 20% of cases. Molecular neuroimaging techniques such as PET have been used for the in vivo assessment of molecular processes at their sites of action, permitting detection of subtle pathophysiological changes in the brain at asymptomatic stages The development of molecular imaging methods for noninvasively assessing disease-specific traits such as Aβ burden in AD is allowing early diagnosis at presymptomatic stages, more accurate differential diagnosis and, when available, the evaluation and monitoring of disease-modifying therapy.
Key findings
- The increasing age of the population in developed countries suggests that, if unchecked, these disorders will become increasingly prevalent.
Why it matters
This review states that evidence supports an imbalance between production and removal of beta-amyloid as central to Alzheimer disease, and that understanding of how beta-amyloid forms and damages neurons is being turned into new treatment approaches. It notes that without specific biologic markers, direct examination of brain tissue is still the only definitive way to diagnose Alzheimer disease and other dementias.
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Study details
- Evidence strengthLow
How this study scored 35/100
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 (PET clinics) |
| Journal's citation record | 0 / 4 | PET Clinics: journal h-index 44 (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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 29 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.6 citations a year over 18 year(s) since 2010 |
| Impact for its field and year | 2 / 6 | Cited 1.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 1 / 4 | Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Christopher Cleon Rowe: h-index 100 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Austin Health: institution h-index 458 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27157482) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 35 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
May need a subscription Unpaywall, Europe PMC and OpenAlex found no free copy of the full text (checked 10 Oct 2026), so the publisher may charge for it. The PubMed abstract is free.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Villemagne, V. L., & Rowe, C. C. (2010). Amyloid PET Ligands for Dementia. PET clinics. https://doi.org/10.1016/j.cpet.2009.12.008
Vancouver
Villemagne VL, Rowe CC. Amyloid PET Ligands for Dementia. PET clinics. 2010. doi:10.1016/j.cpet.2009.12.008. PMID: 27157482.
BibTeX
@article{villemagne2010-27157482,
author = {Villemagne, V. L. and Rowe, C. C.},
title = {{Amyloid PET Ligands for Dementia}},
journal = {PET clinics},
year = {2010},
doi = {10.1016/j.cpet.2009.12.008},
pmid = {27157482},
url = {https://doi.org/10.1016/j.cpet.2009.12.008}
}
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