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Alzheimer's disease
Blennow K, de Leon MJ, Zetterberg H.. Lancet (London, England), 2006-07-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease is the most common cause of dementia. Research advances have enabled detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie, plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated tau. However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide. The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors. This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies.
Key findings
- However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder.
- Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism.
- By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide.
- The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors.
- This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies.
Why it matters
This seminar reviews the epidemiology, genetics, pathogenesis, diagnosis, and treatment of Alzheimer's disease, noting that familial Alzheimer's disease is a very rare autosomal dominant early-onset disease caused by mutations in the amyloid precursor protein and presenilin genes. It states that the cause of the much more common sporadic form is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of genetic and environmental risk factors.
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Study details
- Evidence strengthLow
How this study scored 61/100
Published in a top-tier 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 | 10 / 10 | Tier 1 — top-tier general journal (Lancet (London, England)) |
| Journal's citation record | 4 / 4 | The Lancet: journal h-index 1,205 (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 | 7 / 7 | Cited 3,106 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 141.2 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 6 / 6 | Cited 66.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 90 other studies in this library |
| Still being cited | 4 / 4 | Cited 378 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Henrik Zetterberg: h-index 196 (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 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16876668) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 61 / 100 | — |
What each of these 20 components measures, and what this score is not →
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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
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006). Alzheimer's disease. Lancet (London, England). https://doi.org/10.1016/s0140-6736(06)69113-7
Vancouver
Blennow K, de Leon MJ, Zetterberg H. Alzheimer's disease. Lancet (London, England). 2006. doi:10.1016/s0140-6736(06)69113-7. PMID: 16876668.
BibTeX
@article{blennow2006-16876668,
author = {Blennow, K. and de Leon, M. J. and Zetterberg, H.},
title = {{Alzheimer's disease}},
journal = {Lancet (London, England)},
year = {2006},
doi = {10.1016/s0140-6736(06)69113-7},
pmid = {16876668},
url = {https://doi.org/10.1016/s0140-6736(06)69113-7}
}
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