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Molecular mechanisms for Alzheimer's disease: implications for neuroimaging and therapeutics
Masters CL, Cappai R, Barnham KJ, Villemagne VL.. Journal of neurochemistry, 2006-06-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease is a progressive neurodegenerative disorder characterised by the gradual onset of dementia. The pathological hallmarks of the disease are beta-amyloid (Abeta) plaques, neurofibrillary tangles, synaptic loss and reactive gliosis. The current therapeutic effort is directed towards developing drugs that reduce Abeta burden or toxicity by inhibiting secretase cleavage, Abeta aggregation, Abeta toxicity, Abeta metal interactions or by promoting Abeta clearance. A number of clinical trials are currently in progress based on these different therapeutic strategies and they should indicate which, if any, of these approaches will be efficacious. Current diagnosis of Alzheimer's disease is made by clinical, neuropsychologic and neuroimaging assessments. Routine structural neuroimaging evaluation with computed tomography and magnetic resonance imaging is based on non-specific features such as atrophy, a late feature in the progression of the disease, hence the crucial importance of developing new approaches for early and specific recognition at the prodromal stages of Alzheimer's disease. Functional neuroimaging techniques such as functional magnetic resonance imaging, magnetic resonance spectroscopy, positron emission tomography and single photon emission computed tomography, possibly in conjunction with other related Abeta biomarkers in plasma and CSF, could prove to be valuable in the differential diagnosis of Alzheimer's disease, as well as in assessing prognosis. With the advent of new therapeutic strategies there is increasing interest in the development of magnetic resonance imaging contrast agents and positron emission tomography and single photon emission computed tomography radioligands that will permit the assessment of Abeta burden in vivo.
Key findings
- A number of clinical trials are currently in progress based on these different therapeutic strategies and they should indicate which, if any, of these approaches will be efficacious.
- Current diagnosis of Alzheimer's disease is made by clinical, neuropsychologic and neuroimaging assessments.
- Routine structural neuroimaging evaluation with computed tomography and magnetic resonance imaging is based on non-specific features such as atrophy, a late feature in the progression of the disease, hence the crucial importance of developing new approaches for early and specific recognition at the prodromal stages of Alzheimer's disease.
- Functional neuroimaging techniques such as functional magnetic resonance imaging, magnetic resonance spectroscopy, positron emission tomography and single photon emission computed tomography, possibly in conjunction with other related Abeta biomarkers in plasma and CSF, could prove to be valuable in the differential diagnosis of Alzheimer's disease, as well as in assessing prognosis.
- With the advent of new therapeutic strategies there is increasing interest in the development of magnetic resonance imaging contrast agents and positron emission tomography and single photon emission computed tomography radioligands that will permit the assessment of Abeta burden in vivo.
Why it matters
This review describes therapeutic strategies being tested in clinical trials, such as reducing beta-amyloid burden or toxicity, but states that it is not yet known which approaches will be efficacious. It also notes that current structural neuroimaging relies on late features like atrophy, highlighting the need for earlier and more specific diagnosis.
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Study details
- Evidence strengthLow
How this study scored 46/100
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 (Journal of neurochemistry) |
| Journal's citation record | 3 / 4 | Journal of Neurochemistry: journal h-index 349 (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 | 2006 — older than 20 years, still counted |
| 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 | 5 / 7 | Cited 241 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.0 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 4 / 6 | Cited 11.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 8 other studies in this library |
| Still being cited | 1 / 4 | Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Victor L. Villemagne: h-index 110 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | The University of Melbourne: institution h-index 1,342 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16805778) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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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
Masters, C. L., Cappai, R., Barnham, K. J., & Villemagne, V. L. (2006). Molecular mechanisms for Alzheimer's disease: implications for neuroimaging and therapeutics. Journal of neurochemistry. https://doi.org/10.1111/j.1471-4159.2006.03989.x
Vancouver
Masters CL, Cappai R, Barnham KJ, Villemagne VL. Molecular mechanisms for Alzheimer's disease: implications for neuroimaging and therapeutics. Journal of neurochemistry. 2006. doi:10.1111/j.1471-4159.2006.03989.x. PMID: 16805778.
BibTeX
@article{masters2006-16805778,
author = {Masters, C. L. and Cappai, R. and Barnham, K. J. and Villemagne, V. L.},
title = {{Molecular mechanisms for Alzheimer's disease: implications for neuroimaging and therapeutics}},
journal = {Journal of neurochemistry},
year = {2006},
doi = {10.1111/j.1471-4159.2006.03989.x},
pmid = {16805778},
url = {https://doi.org/10.1111/j.1471-4159.2006.03989.x}
}
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