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Research

32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–17 of 17 studies in Biomarkers in The Lancet. Neurology · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 17 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 17,651 studies have no institution on record and are not counted here.

What “Biomarkers” covers

Biomarkers — Measurable signals in blood, brain scans or spinal fluid that can indicate Alzheimer's changes.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

CSF and blood biomarkers for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis

✓ Peer-reviewed alzhub usefulness score 81 out of 100. The Lancet. Neurology 2016-04-08

The core biomarkers differentiated Alzheimer's disease from controls with good performance: CSF T-tau (average ratio 2·54, 95% CI 2·44-2·64, p Interpretation The core CSF biomarkers of neurodegeneration (T-tau, P-tau, and Aβ42), CSF NFL, and plasma T-tau were strongly associated with Alzheimer's disease and the core biomarkers were strongly associated with mild cognitive impairment due to Alzheimer's disease. 2 key findings →

Design: systematic review Participants: 699 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Blood phosphorylated tau for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis

✓ Peer-reviewed alzhub usefulness score 76 out of 100. The Lancet Neurology 2025-09

This large review pooled 113 studies (nearly 30,000 people) comparing different forms of blood phosphorylated tau for detecting Alzheimer's pathology. p-tau217 was clearly the best-performing marker, correctly identifying disease pathology about 88% of the time, outperforming other tau variants like p-tau181. 4 key findings →

Design: meta-analysis Participants: 29,625 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Integration of plasma eMTBR-tau243 and p-tau217 in the diagnosis and stratification of Alzheimer's disease: a prospective cohort study

✓ Peer-reviewed alzhub usefulness score 72 out of 100. The Lancet. Neurology 2026-04

In this prospective cohort study, we included adults aged 40 years or older with subjective cognitive decline, mild cognitive impairment, or dementia, based on cognitive test results and clinical assessments, consecutively recruited at two memory clinics in Sweden, as part of the Swedish BioFINDER-2 study. 3 key findings →

Design: cohort Participants: 572 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Blood phosphorylated tau for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis

✓ Peer-reviewed alzhub usefulness score 72 out of 100. The Lancet. Neurology 2025-09-01

Plasma p-tau217 was the highest-performing biomarker for identifying biologically defined Alzheimer's disease, with pooled sensitivity of 88·1% (95% CI 86·7-89·5, moderate certainty of evidence), specificity of 88·7% (87·4-89·9, moderate certainty of evidence), area under the receiver operating characteristic curve (AUROC) of 91·1% (88·9-92·4, moderate certainty of evidence), and diagnostic odds ratio of 50·7 (40·6-63·4). p-tau181 pooled sensitivity was 80·5% (78·4-82·4, low certainty of evidence), specificity was 76·4% (74·1-78·6, low certainty of evidence), AUROC was 81·5% (80·2-82·9, low certainty of evidence), and diagnostic odds ratio was 13·4 (11·4-16·7). p-tau205 pooled sensitivity was 76·6% (70·7-81·6, moderate certainty of evidence), specificity was 86·0% (78·6-91·2, moderate certainty of evidence), AUROC was 85·1% (80·7-89·6, moderate certainty of evidence), and diagnostic odds ratio was 20·2 (10·5-38·7). p-tau212 pooled sensitivity was 84·5% (75·5-90·6, moderate certainty of evidence), specificity was 87·3% (79·5-92·5, moderate certainty of evidence), AUROC was 90·3% (86·6-94·1, moderate certainty of evidence), and diagnostic odds ratio was 41·2 (22·0-77·3). p-tau231 pooled sensitivity was 75·2% (71·3-78·8, moderate certainty of evidence), specificity was 75·3% (71·2-78·9, moderate certainty of evidence), AUROC was 80·2 (77·6-82·7, moderate certainty of evidence), and diagnostic odds ratio was 9·3 (7·0-12·2). 4 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source

Prediction of amyloid and tau brain deposition and cognitive decline in people with Down syndrome using plasma biomarkers: a longitudinal cohort study

✓ Peer-reviewed alzhub usefulness score 72 out of 100. The Lancet. Neurology 2025-07-01

Baseline p-tau217, as well as GFAP, NfL, or t-tau, were individually associated with longitudinal changes in DS-MSE, Aβ-PET, and tau-PET, and with progression to dementia. 5 key findings →

Design: cohort study Participants: 220 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Associations between blood pressure across adulthood and late-life brain structure and pathology in the neuroscience substudy of the 1946 British birth cohort (Insight 46): an epidemiological study

✓ Peer-reviewed alzhub usefulness score 71 out of 100. The Lancet. Neurology 2019-08-20

High and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69-71 years of age. 5 key findings →

Design: longitudinal study Participants: 5,362 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Comparison of tau spread in people with Down syndrome versus autosomal-dominant Alzheimer's disease: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 67 out of 100. The Lancet. Neurology 2024-05-01

Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →

Design: cohort study Participants: 137 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Plasma and CSF biomarkers for the diagnosis of Alzheimer's disease in adults with Down syndrome: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 64 out of 100. The Lancet. Neurology 2018-08-29

The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group. 4 key findings →

Design: cross-sectional Participants: 282 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Serum neurofilament light chain in genetic frontotemporal dementia: a longitudinal, multicentre cohort study

✓ Peer-reviewed alzhub usefulness score 64 out of 100. The Lancet. Neurology 2019-12-01

Baseline NfL was elevated in symptomatic carriers (median 52 pg/mL [IQR 24-69]) compared with presymptomatic carriers (9 pg/mL [6-13]; p<0·0001) and non-carriers (8 pg/mL [6-11]; p<0·0001), and was higher in converters than in non-converting carriers (19 pg/mL [17-28] vs 8 pg/mL [6-11]; p=0·0007; adjusted for age). 4 key findings →

Design: cohort study Participants: 59 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Plasma neurofilament light chain in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional and longitudinal cohort study

✓ Peer-reviewed alzhub usefulness score 63 out of 100. The Lancet. Neurology 2020-05-26

We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →

Design: cohort study Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Comparison of CSF biomarkers in Down syndrome and autosomal dominant Alzheimer's disease: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 62 out of 100. The Lancet. Neurology 2021-08-01

Due to trisomy of chromosome 21 and the resultant extra copy of the amyloid precursor protein gene, nearly all adults with Down syndrome develop Alzheimer's disease pathology by the age of 40 years and are at high risk for dementia given their increased life expectancy compared with adults with Down syndrome in the past. 1 key finding →

Design: cross-sectional Participants: 41 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Comparison of amyloid burden in individuals with Down syndrome versus autosomal dominant Alzheimer's disease: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 60 out of 100. The Lancet. Neurology 2023-01-01

Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. 2 key findings →

Design: cross-sectional Participants: 216 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Plasma phosphorylated tau 217 concentrations, APOE genotype, and timing of cognitive impairment in individuals across diverse racial and ethnic groups: a pooled analysis of prospective cohort studies

✓ Peer-reviewed alzhub usefulness score 59 out of 100. The Lancet. Neurology 2026-09-09

Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →

Design: cohort Participants: 8,582 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Dynamic changes in plasma biomarkers of Alzheimer's disease in patients treated with lecanemab: a longitudinal cohort study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Lancet Neurology 2026-09-01

The study included 197 patients in whom lecanemab infusions had been started (lecanemab group), as well as 173 patients in whom lecanemab had been ordered but not yet started, who were combined with 1139 research participants with cognitive impairment from the Knight ADRC cohort to form the untreated control group with cognitive impairment (n=1312). 5 key findings →

Design: cohort study Participants: 1,312 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomized / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multicenter collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 32,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,045 records (3.2% of the library) are not peer-reviewed — 966 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events

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