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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Getting a diagnosis

Topic: Amyloid, tau and blood-test diagnosis

Although the prevalence of dementia continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health. Alzheimer's disease, the most prevalent cause of dementia, is still defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality as proposed in the original amyloid hypothesis. Age-related, protective, and disease-promoting factors probably interact with the core mechanisms of the disease. Amyloid β42, and tau proteins are established core cerebrospinal biomarkers; novel candidate biomarkers include amyloid β oligomers and synaptic markers. MRI and fluorodeoxyglucose PET are established imaging techniques for diagnosis of Alzheimer's disease. Amyloid PET is gaining traction in the clinical arena, but validity and cost-effectiveness remain to be established. Tau PET might offer new insights and be of great help in differential diagnosis and selection of patients for trials. In the search for understanding the disease mechanism and keys to treatment, research is moving increasingly into the earliest phase of disease. Preclinical Alzheimer's disease is defined as biomarker evidence of Alzheimer's pathological changes in cognitively healthy individuals. Patients with subjective cognitive decline have been identified as a useful population in whom to look for preclinical Alzheimer's disease. Moderately positive results for interventions targeting several lifestyle factors in non-demented elderly patients and moderately positive interim results for lowering amyloid in pre-dementia Alzheimer's disease suggest that, ultimately, there will be a future in which specific anti-Alzheimer's therapy will be combined with lifestyle interventions targeting general brain health to jointly combat the disease. In this Seminar, we discuss the main developments in Alzheimer's research.

Key findings

Why it matters

This review notes that although dementia prevalence continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health, and that researchers are moving away from the simple linear causality of the original amyloid hypothesis. It reports moderately positive results for interventions targeting several lifestyle factors in non-demented elderly patients and moderately positive interim results for lowering amyloid in pre-dementia Alzheimer's disease.

Study details

How this study scored 64/100
How this study's score is builtJournal tier 10 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 7 of 7; Citations per year 5 of 5; Impact for its field and year 6 of 6; Cited by studies here 5 of 6; Still being cited 4 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 3 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 64 of 100.64 of 100 points earned36 not earned

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.

ComponentPointsWhy
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 2016 — 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 7 / 7 Cited 3,117 times (OpenAlex, 2026-10-10)
Citations per year 5 / 5 259.8 citations a year over 12 year(s) since 2016
Impact for its field and year 6 / 6 Cited 233.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 5 / 6 Cited by 112 other studies in this library
Still being cited 4 / 4 Cited 771 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Wiesje M. van der Flier: h-index 132 (OpenAlex, whole career)
Institution's track record 2 / 3 University College London: institution h-index 2,029 (OpenAlex)
Multi-centre collaboration 3 / 3 OpenAlex lists 11 institution(s) in 8 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 26921134)
Free to read 0 / 2 Behind a paywall — scores zero
Total 64 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), 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. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

APA 7th

Scheltens, P., Blennow, K., Breteler, M. M., de Strooper, B., Frisoni, G. B., Salloway, S., et al. (2016). Alzheimer's disease. Lancet (London, England). https://doi.org/10.1016/s0140-6736(15)01124-1

Vancouver

Scheltens P, Blennow K, Breteler MM, de Strooper B, Frisoni GB, Salloway S, et al. Alzheimer's disease. Lancet (London, England). 2016. doi:10.1016/s0140-6736(15)01124-1. PMID: 26921134.

BibTeX

@article{scheltens2016-26921134,
  author  = {Scheltens, P. and Blennow, K. and Breteler, M. M. and de Strooper, B. and Frisoni, G. B. and Salloway, S. and Van der Flier, W. M.},
  title   = {{Alzheimer's disease}},
  journal = {Lancet (London, England)},
  year    = {2016},
  doi     = {10.1016/s0140-6736(15)01124-1},
  pmid    = {26921134},
  url     = {https://doi.org/10.1016/s0140-6736(15)01124-1}
}

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