Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

Showing 1–25 of 246 studies in Biomarkers of type cross-sectional study (page 1 of 10) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 246 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.

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.

In a cross-sectional analysis of 26 individuals, bifrontal cortical FDG hypometabolism was associated with worse Clinical Dementia Rating (CDR) plus National Alzheimer's Coordinating Center frontotemporal lobar degeneration sum of boxes score (b = -3.6 × 10-2 standardized uptake value ratio [SUVR] units/CDR units; 95% CI, -4.9 × 10-2 to -2.2 × 10-2; P < .001), high cerebrospinal fluid NfL (b = -9.2 × 10-5 SUVR units/pg NfL/mL; 95% CI, -1.3 × 10-4 to -5.6 × 10-5; P < .001), and high CSF t-tau (-7.2 × 10-4 SUVR units/pg t-tau/mL; 95% CI, -1.4 × 10-3 to -9.5 × 10-5; P = .03). 2 key findings →

Design: cross-sectional Participants: 27 Evidence: high

Discriminative Accuracy of Plasma Phospho-tau217 for Alzheimer Disease vs Other Neurodegenerative Disorders

✓ Peer-reviewed alzhub usefulness score 77 out of 100. JAMA 2020-08-01

Mean age was 83.5 (SD, 8.5) years in cohort 1, 69.1 (SD, 10.3) years in cohort 2, and 35.8 (SD, 10.7) years in cohort 3; 38% were women in cohort 1, 51% in cohort 2, and 57% in cohort 3. 4 key findings →

Design: cross-sectional Participants: 301 Evidence: moderate

This study suggests that plasma GFAP is a sensitive biomarker for detecting and tracking reactive astrogliosis and Aβ pathology even among individuals in the early stages of AD. 5 key findings →

Design: cross-sectional Participants: 300 Evidence: moderate

Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. 2 key findings →

Design: cross-sectional Participants: 187 Evidence: moderate

Plasma Phosphorylated Tau 217 to Identify Preclinical Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 72 out of 100. JAMA Neurology 2025-11-01

Participants had a mean (SD) age of 66.9 (9.9) years; 971 (33.3%) were Aβ positive by either CSF or PET, 1667 (57.2%) were women, and 1108 (38.1%) carried at least 1 APOE ε4 allele. 5 key findings →

Design: cross-sectional Participants: 2,916 Evidence: high

Plasma p-tau217/Aβ42 has high performance in detecting cerebral AD pathologies, thus offering a promising tool for clinical diagnosis and community screening of AD. 1 key finding →

Design: cross-sectional Participants: 512 Evidence: moderate

The mean (SD) age of the 842 participants in cohort 1 was 72 (5.6) years, with a range of 59 to 88 years, and 446 (52.5%) were female. 3 key findings →

Design: cross-sectional Participants: 842 Evidence: moderate

For all 4 phosphorylation sites assessed in CSF, p-tau was significantly more closely associated with amyloid-PET values than tau-PET values (p-tau181 difference, 13%; 95% CI, 3%-22%; P = .006; p-tau217 difference, 11%; 95% CI, 3%-20%; P = .003; p-tau231 difference, 15%; 95% CI, 5%-22%; P Conclusions and relevance Results of this cross-sectional study of 2 observational cohorts suggest that the p-tau abnormality as an early event in AD pathogenesis was associated with amyloid-β accumulation and highlights the need for careful interpretation of p-tau biomarkers in the context of the amyloid/tau/neurodegeneration, or A/T/(N), framework. 2 key findings →

Design: cross-sectional Participants: 609 Evidence: moderate

Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum

✓ Peer-reviewed alzhub usefulness score 70 out of 100. JAMA neurology 2022-03-01

This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. 3 key findings →

Design: cross-sectional Participants: 97 Evidence: moderate

Quantitative Assessment of the Effect of Chronic Kidney Disease on Plasma P-Tau217 Concentrations

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurology 2025-01-17

CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →

Design: cross-sectional Participants: 202 Evidence: moderate

Higher eGFR was associated with increased levels of plasma p-tau217, p-tau181, Tau212-221, and Tau181-190 in individuals with cognitive impairment (cohort 1: R range, -0.24 to -0.59; P Conclusions and relevance In this study, CKD was associated with increased plasma levels of soluble tau, but for p-tau217 the associations were considerably lower than the association with Aβ positivity. 4 key findings →

Design: cross-sectional Participants: 141 Evidence: moderate

Overall the study included 199 participants with iRBD, 20 hyposmic participants with available dopamine transporter single-photon emission computed tomography, 146 nonmanifest GBA1N409S gene carriers, 21 GBA1N409S gene carrier patients with PD, 50 patients with sporadic PD, and 140 healthy controls. 3 key findings →

Design: cross-sectional Participants: 170 Evidence: low

A total of 428 participants were included; 167 had normal cognition, 245 had MCI, and 16 had mild AD. 2 key findings →

Design: cross-sectional Participants: 428 Evidence: moderate

Diagnosis of cognitive impairment and dementia: blood plasma and optical coherence tomography

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Brain communications 2024-12-27

After adjusting for retinal scan signal strength, neurofilament light chain showed a stronger negative association with retinal nerve fibre layer thickness [standardized beta estimate ( β ) = -0.184] and ganglion cell-inner plexiform layer thickness ( β = -0.139) compared to phosphorylated tau181, which exhibited weaker associations with ganglion cell-inner plexiform layer ( β = -0.091) and retinal nerve fibre layer ( β = -0.059). 3 key findings →

Design: cross-sectional Participants: 100 Evidence: low

Blood Biomarkers to Detect Alzheimer Disease in Primary Care and Secondary Care

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA 2024-10-15

This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →

Design: cross-sectional Participants: 1,213 Evidence: high

This large multi-country study tested a fully automated, commercially available blood test (Lumipulse platform, measuring p-tau217) in nearly 1,800 people across memory clinics and, notably, primary care doctors' offices in Sweden, Spain, and Italy. 5 key findings →

Design: cross-sectional Participants: 1,767 Evidence: high

Association of Factors With Elevated Amyloid Burden in Clinically Normal Older Individuals

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA neurology 2020-06-01

The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid. 5 key findings →

Design: cross-sectional Participants: 4,486 Evidence: low

Evaluation of the Revised Criteria for Biological and Clinical Staging of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA neurology 2025-07-01

There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included. 3 key findings →

Design: cross-sectional Participants: 838 Evidence: moderate

P-tau181 (odds ratio [OR] 2.06, 95% confidence interval [CI] 1.41-3.00, p < 0.001), p-tau217 (OR 1.70, 95% CI 1.10-2.61, p = 0.016), and t-tau (OR 1.44, 95% CI 1.08-1.92, p = 0.012) were associated with appetite change. 5 key findings →

Design: cross-sectional Participants: 1,005 Evidence: low

We included 400 middle-aged CU participants, of whom 135 (33.8%) were CSF Aβ-positive. 5 key findings →

Design: cross-sectional Participants: 400 Evidence: moderate

Our results demonstrate the feasibility and potential of immunoassay-based multiplexing to provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework. 5 key findings →

Design: cross-sectional Participants: 113 Evidence: moderate

↑ Change the filters

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
  • Randomised / 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
  • Multi-centre 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% of the library) are not peer-reviewed — 962 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