BAN2401-G000-201 did not meet the 12-month primary endpoint. 5 key findings →
Design: clinical trial Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Patients with MCI with APOEε4, abnormal CSF τ level, hippocampal and medial temporal lobe atrophy, entorhinal atrophy, depression, diabetes, hypertension, older age, female gender, lower MMSE score and higher ADAS-cog score, had a high risk for the progression to AD. 1 key finding →
Design: meta-analysis Participants: 14,821 Evidence: high
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
Association of HT use and risk of AD may depend on timing of use. 4 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
ADCOMS is proposed as new standard outcome for pAD and mild AD dementia trials, and is progressing in a CAMD-sponsored qualification process for use in registration trials of pAD. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this cohort and MR study of UK Biobank participants, cataracts were associated with increased risk of dementia, especially vascular dementia, and reduced total brain volumes. 5 key findings →
Design: cohort Participants: 304,953 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
65/100
This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study Participants: 271 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To evaluate reverse causation, we assessed whether a polygenic risk score for AD is associated with HGS. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Diabetes and even prediabetes are associated with accelerated brain aging, especially among men and people with poor cardiometabolic health. 4 key findings →
Participants: 31,229 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
At baseline, participants (n = 168) were cognitively normal and primarily middle-aged (mean 56.4 years, SD 10.9 years) and had both vascular risk factor status and proximal CSF biomarkers available. 4 key findings →
Design: cohort study Participants: 168 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma GFAP and pTau biomarkers (pTau181, pTau231, pTau217) are significantly elevated in Aβ-positive individuals, with stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181). 5 key findings →
Design: cohort Participants: 806 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
59/100
International hospital-based studies have indicated a high risk of cognitive impairment after stroke, evidence from community-based studies in China is scarce. 2 key findings →
Design: cross-sectional Participants: 599 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The gap between predicted brain age using magnetic resonance imaging (MRI) and chronological age may serve as a biomarker for early-stage neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Loss-of-function (LOF) variants of TREM2, an immune receptor expressed in microglia, increase Alzheimer's disease risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ApoE4, a strong genetic risk factor for Alzheimer disease, has been associated with increased risk for severe COVID-19. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The estimated total annual costs of dementia in China increased from 0.9 billion United States dollars (US$) in 1990 to US$ 47.2 billion in 2010 and were predicted to reach US$ 69.0 billion in 2020 and US$ 114.2 billion in 2030. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nicotinamide adenine dinucleotide (NAD)+-dependent sirtuins have been identified to be key regulators in the lifespan extending effects of calorie restriction (CR) in a number of species. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein that is predominantly expressed by microglia in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study investigated whether longitudinal changes in CSF AD biomarkers were associated with 18 F-MK6240 tau PET measures in early Braak stage subregions. 4 key findings →
Design: cross-sectional Participants: 78 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The association of rs1990622 with AAO explains, in part, the wide range in the AAO of disease among GRN mutation carriers. 3 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mitochondrial dysfunction and oxidative stress occur in vascular dementia (VaD), but the specific molecular mechanism regulating these events remains unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to investigate whether spicy food consumption is associated with cognition and cerebrospinal fluid (CSF) biomarkers of AD in the Chinese population. 4 key findings →
Design: case-control study Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder; it is the most common cause of dementia and has no treatment. 4 key findings →
Evidence: low
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.
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →