CSF p-tau181 and p-tau231 biomarkers distinguished AD, MCI, and healthy populations. 2 key findings →
Participants: 5,017 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our findings suggest that mid-life serum AD biomarkers could be associated with accelerated cognitive decline from mid- to late life in women. 5 key findings →
Design: longitudinal study Participants: 192 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In community and clinical settings, SCC predict both dementia and depression in the absence of dementia. 3 key findings →
Design: case-control study Participants: 6,357 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparable performance of CSF and blood NfL in many groups demonstrates the promise of NfL as a noninvasive biomarker of neurodegeneration; however, its utility in clinically meaningful scenarios requires greater scrutiny. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Study objectives To investigate the cumulative effect of five consecutive nights of partial sleep deprivation (PSD) on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults. 1 key finding →
Participants: 13 Evidence: high
Full summary, score breakdown and related studies → Original source
In our study, in addition to PD, NFL was suggested to be a global diagnostic biomarker for neurodegenerative diseases. 4 key findings →
Design: meta-analysis Participants: 36 Evidence: high
Full summary, score breakdown and related studies → Original source
72/100
At present we cannot recommend CSF NfH and NfL levels for use as a screening test in the diagnosis of dementia because of the rather small effect size. 2 key findings →
Design: systematic review Participants: 818 Evidence: high
Full summary, score breakdown and related studies → Original source
This study suggests that plasma Aβ42/Aβ40, as determined by this MS-based assay, has potential value as an accurate and cost-effective tool to identify individuals in the earliest stages of AD, supporting its implementation in clinical trials, preventative strategies and clinical practice. 5 key findings →
Design: cohort study Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The distribution of tau pathology in Alzheimer's disease (AD) shows remarkable inter-individual heterogeneity, including hemispheric asymmetry. 1 key finding →
Design: longitudinal study Participants: 102 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings suggest that C 2 N Diagnostics' MS-based plasma biomarkers can detect brain amyloid and tau with high accuracy prior to dementia and could aid in identifying candidates for clinical trials or therapeutic intervention. 5 key findings →
Design: cohort study Participants: 304 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This landmark NIH-funded trial (REACH II) tested a structured, multi-part support program for 642 Hispanic, White, and Black family caregivers of people with Alzheimer's or related dementias across 5 U.S. cities. 4 key findings →
Design: RCT Participants: 642 Evidence: high
Full summary, score breakdown and related studies → Original source
In a study of 2.2 million adults in Ontario, Canada, people who lived very close to a major road (within 50 meters) had a small but statistically significant higher risk of developing dementia than those living farther away (over 300 meters), even after accounting for other health and demographic factors. 4 key findings →
Design: cohort Participants: 2,200,000 Evidence: high
Full summary, score breakdown and related studies → Original source
The most significant adverse events associated with these therapies are infusion-related reactions and amyloid-related imaging abnormalities (ARIA) with edema/effusion (ARIA-E) and/or hemorrhage/hemosiderin deposition (ARIA-H). 5 key findings →
Design: cohort Participants: 234 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
More frequent social contact at age 60 years was associated with lower dementia risk (hazard ratio [HR] for each SD higher social contact frequency = 0.88 [95% CI 0.79, 0.98], p = 0.02); effect size of the association of social contact at 50 or 70 years with dementia was similar (0.92 [95% CI 0.83, 1.02], p = 0.13 and 0.91 [95% CI 0.78, 1.06], p = 0.23, respectively) but not statistically significant. 3 key findings →
Design: cohort Participants: 10,228 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across the cohorts, each 10-year increase in BAI was associated with a 39% higher risk of incident dementia (hazard ratio [HR], 1.39 [95% CI, 1.21-1.59]; P Conclusions and relevance In this IPD meta-analysis, a higher sleep EEG-based BAI was associated with a higher risk of incident dementia. 3 key findings →
Design: meta-analysis Participants: 7,105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau plays a key role in Alzheimer's disease (AD) pathophysiology, and accumulating evidence suggests that lowering tau may reduce this pathology. 1 key finding →
Design: phase-1-trial Participants: 46 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →
Design: cohort Participants: 139 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Participants receiving CDCM showed significantly fewer behavioral and psychological symptoms (adjusted mean difference [AMD] in NPI score, -10.26 [95% CI, -16.95 to -3.58]; P = .003; Cohen d, -0.78 [95% CI, -1.09 to -0.46]), better mental health (AMD in SF-12 Mental Component Summary score, 2.26 [95% CI, 0.31-4.21]; P = .02; Cohen d, 0.26 [95% CI, -0.11 to 0.51]), and lower caregiver burden (AMD in BIZA-D score, -0.59 [95% CI, -0.81 to -0.37]; P Conclusions and relevance In this secondary analysis of a cluster randomized clinical trial, CDCM was associated with improved patient, caregiver, and health system-relevant outcomes over 36 months beyond the intervention period. 3 key findings →
Design: RCT Participants: 428 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Glymphatic failure may precede amyloid pathology, and predicts amyloid deposition, neurodegeneration, and clinical progression in AD. 2 key findings →
Design: cohort Participants: 419 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
These two conclusions support a dynamic biomarker model in which Alzheimer's disease is characterized first by the appearance of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associated with clinical symptoms. 1 key finding →
Design: longitudinal study Participants: 1,343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. 3 key findings →
Design: meta-analysis Participants: 3,154 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →