27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →
Design: cross-sectional Participants: 995 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A reliable method of detecting Alzheimer disease (AD) in its prodromal state is needed for patient stratification in clinical trials or for personalizing existing or potential upcoming therapies. 4 key findings →
Design: cohort study Participants: 928 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma markers have been reported to be associated with brain amyloid burden, tau pathology, or neurodegeneration. 4 key findings →
Design: cross-sectional Participants: 183 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
's ≥ 0.75). Both markers identified Braak stage V-VI levels with similarly high performance (entorhinal SUVR, area under the curve [AUC] = 0.92 [95% CI 0.91-0.93]; temporal meta-ROI SUVR, AUC = 0.91 [95% CI 0.90-0.92]; plasma p-tau217, AUC = 0.90 [95% CI 0.89-0.91]), but PET outperformed plasma p-tau217 in identifying high/intermediate ADNCs (entorhinal ROI, AUC = 0.94 [95% CI 0.94-0.95]; temporal meta-ROI AUC = 0.94 [95% CI 0.94-0.95]; plasma p-tau217, AUC = 0.89 [95% CI 0.88-0.90]). 2 key findings →
Participants: 56 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In 272 participants, mean (SD) age was 70 (4.5) years, 270 were male (99.3%), and 83 (30.5%) were amyloid-PET positive. 5 key findings →
Design: cohort study Participants: 272 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
-fold changes of 1.21, 0.57, and 4.63, respectively, compared to A-. 5 key findings →
Design: cross-sectional Participants: 252 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 1,345 individuals were included. 5 key findings →
Design: cohort study Participants: 1,345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This review discusses time-dependent models of Alzheimer's disease (AD) that track the temporal evolution of validated pathophysiological biomarkers relative to age of onset, aging, and co-occurring brain pathologies. 4 key findings →
Full summary, score breakdown and related studies → Original source Free full text
This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders. 2 key findings →
Full summary, score breakdown and related studies → Original source Free full text
The optimal cut-offs differed between CU and CI groups. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →
Design: cross-sectional Participants: 605 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CSF NFL differs among different neurodegenerative diseases and is especially high in dementias engaging subcortical brain regions, such as VaD and mixed AD and VaD, but also in frontotemporal dementia. 1 key finding →
Participants: 478 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Plasma GFAP alone differentiates AD from FTD and neurodegenerative dementias from HC but with lower accuracy than p-tau181 and NfL. 3 key findings →
Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In women, increased plasma adiponectin levels are an independent risk factor for the development of both all-cause dementia and AD. 3 key findings →
Design: cohort study Participants: 159 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biomarker trajectory shapes by MMSE score were complex and were affected by interactions with age and APOE status. 3 key findings →
Design: cross-sectional Participants: 343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The CSF levels of Aβ42 but not total and phosphorylated tau were lower in APOE ε4 carriers compared with noncarriers irrespective of diagnostic group (cohort A). 3 key findings →
Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Furthermore, the CSF biomarker analyses provide a first insight into the potentially predominant pathogenetic mechanism(s) underlying the association between AD risk and PICALM. 1 key finding →
Design: case-control study Participants: 4,254 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Subtle memory impairment with a positive β-amyloid scan identifies healthy individuals at high risk for MCI or AD. 3 key findings →
Participants: 87 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Early diagnosis of Alzheimer's disease (AD) is needed to initiate symptomatic treatment with acetylcholinesterase inhibitors, and will be of even greater significance if drugs aimed at slowing down the degenerative process, such as vaccination regimes and beta-secretase and gamma-secretase inhibitors, prove to affect AD pathology and to have clinical effect. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Elevated CSF tau levels are associated with AD pathology and can help discriminate AD from other dementing disorders. 3 key findings →
Participants: 74 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These findings suggest that CSF VILIP-1 and VILIP-1/Aβ42 offer diagnostic utility for early AD, and can predict future cognitive impairment in cognitively normal individuals similarly to tau and tau/Aβ42, respectively. 3 key findings →
Participants: 211 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD. 5 key findings →
Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD), the most common form of dementia, shares many aspects of abnormal brain aging. 2 key findings →
Participants: 195 Evidence: low
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 →