27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The neuropathological confirmation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles (NFT) remains the gold standard for a definitive diagnosis of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 115 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Whilst cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers for amyloid-β (Aβ) and tau pathologies are accurate for the diagnosis of Alzheimer's disease (AD), their broad implementation in clinical and trial settings are restricted by high cost and limited accessibility. 3 key findings →
Design: longitudinal study Participants: 1,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Age, sex, and apolipoprotein E (APOE) are the strongest risk factors for late-onset Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Participants: 4,592 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We identified that combining plasma p-tau217 and a brief cognitive composite score was strongly related to greater risk of progression to AD dementia in MCI patients, suggesting that these measures could be key components of future prognostic algorithms for early AD. 2 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Antibody administration was well tolerated with doses up to 400 mg weekly. 2 key findings →
Design: clinical trial Participants: 52 Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma p-tau 217 and the NfL/p-tau 217 ratio are promising non-invasive biomarkers for differentiating AD from FTLD, suggesting their use as a potential alternative to traditional diagnostic methods. 2 key findings →
Design: cohort study Participants: 374 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma pTau217 is effective for predicting A/T biomarker profile and cognitive decline, though further study is needed to better explain its association with Aβ and tau PET staging. 3 key findings →
Design: longitudinal study Participants: 2,919 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Regardless of the laboratory technique, blood p-tau181 reliably differentiates A+ and A- subjects. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Among 193 cognitively healthy controls, 197 patients with mild cognitive impairment, and 180 patients with AD with dementia, plasma NFL correlated with CSF NFL (Spearman ρ = 0.59, P Conclusions and relevance Plasma NFL is associated with AD diagnosis and with cognitive, biochemical, and imaging hallmarks of the disease. 3 key findings →
Design: case-control study Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Of 490 participants, 251 were women (51.2%) and the mean (SD) age was 65.9 (13.1) years. 4 key findings →
Design: cohort study Participants: 225 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Exclusion criteria included any significant neurologic disorder other than suspected AD; presence of infection, infarction, or multiple lacunes as detected by magnetic resonance imaging; and any significant systemic condition that could lead to difficulty complying with the protocol. 3 key findings →
Design: cohort study Participants: 1,113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau181 (P-tau181) might be increased in Alzheimer's disease (AD), but its usefulness for differential diagnosis and prognosis is unclear. 2 key findings →
Participants: 589 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
During follow-up, 271 participants with MCI were diagnosed with AD and 59 with other dementias. 2 key findings →
Design: cohort study Participants: 750 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cerebrospinal fluid (CSF) p-tau181 (tau phosphorylated at threonine 181) is an established biomarker of Alzheimer's disease (AD), reflecting abnormal tau metabolism in the brain. 3 key findings →
Design: longitudinal study Participants: 194 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. 2 key findings →
Design: longitudinal study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Short term (26 weeks) tideglusib was acceptably safe but produced no clinical benefit in this trial. 4 key findings →
Participants: 86 Evidence: high
Full summary, score breakdown and related studies → Original source
Inclusion criteria were early AD (mini-mental state examination [MMSE] score between 20 and 26 points or Alzheimer's disease assessment scale-cognitive subscale (ADAS-cog) score between 10 and 25 points), taking a stable dose of acetylcholinesterase inhibitor (donepezil, galantamine, or rivastigmine) for at least 4 months, a modified Hachinski score of 4 points or less, and CT or MRI results that were consistent with AD. 3 key findings →
Design: randomized controlled trial Participants: 78 Evidence: high
Full summary, score breakdown and related studies → Original source
Donanemab-mediated slowing of disease progression occurred across baseline tau PET and plasma P-tau217 levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer's dementia (AD) in clinical settings. 3 key findings →
Design: cohort study Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
During 11 years of follow-up, women were 96% more likely than men to be diagnosed with clinical AD dementia after adjusting for age and education in the younger age group 60 to 70 years (n = 946; 95% confidence interval [CI], 1.08 to 3.56) although not in the older age group (70+) (n = 452; hazard ratio = 0.98; 95% CI, 0.68 to 1.53). 5 key findings →
Design: longitudinal study Participants: 1,398 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline sleep disturbance was associated with a faster rate of longitudinal CSF Aβ42 decline. 4 key findings →
Design: longitudinal study Participants: 1,205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of quantitative endophenotypes in genetic studies may provide greater power, allowing for the use of powerful statistical methods and a biological model for the effects of the disease-associated genetic variation. 1 key finding →
Design: meta-analysis Participants: 313 Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma pTau217R matched CSF eMTBR-tau243 and outperformed MTBR-tau243. 5 key findings →
Participants: 242 Evidence: low
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,069 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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
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.
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 27,780 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →