28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The proteins that are found to be altered in the CSF of patients with AD could be used for monitoring disease progression and therapeutic response and perhaps also for early detection once they are validated in larger studies. 3 key findings →
Participants: 2,327 Evidence: low
Full summary, score breakdown and related studies → Original source
The data derived from this patient cohort demonstrate the safety and tolerability of sustained NGF release by a second-generation NGF-ECB implant to the basal forebrain, with uneventful surgical implant and removal of NGF-ECB implants in a new dosing cohort of four patients with AD. 2 key findings →
Design: open-label trial Evidence: moderate
Full summary, score breakdown and related studies → Original source
The role of sAPP isoforms in iNPH seems to be independent from the amyloid cascade. 2 key findings →
Participants: 102 Evidence: low
Full summary, score breakdown and related studies → Original source
The combination of the CSF biomarkers T-tau, Aβ40 and MCP-1 separates iNPH from cognitive and movement disorders with good diagnostic sensitivity and specificity. 1 key finding →
Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source
Concentrations of Aβ 40 and Aβ 42 were much higher in adults with DS than in other groups, reflecting APP gene triplication, while no difference in the Aβ 42 /Aβ 40 ratio between those with DS and sAD may indicate similar processing and deposition of Aβ 40 and Aβ 42 in these groups. 4 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes are fundamental in neural functioning and homeostasis in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicate that SOMAscan performs as well as immunoassay approaches for NfL, Neurogranin, VILIP-1, and sTREM2. 4 key findings →
Participants: 689 Evidence: low
Full summary, score breakdown and related studies → Original source
We conclude that the Aβ 37/42 ratio sensitively detects presenilin/γ-secretase dysfunction and better distinguishes CN from AD than Aβ42/40 in CSF. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The measurement of plasma Aβ peptides with an immunological assay can be improved by preconcentration via immunoprecipitation with an antibody against the Aβ amino-terminus and elution of the captured peptides by heating in a mild detergent-containing buffer. 3 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
A highly robust assay for repeatedly measuring Abeta forms in plasma such as INNO-BIA plasma Abeta forms might be a useful tool in a future risk assessment of AD. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. 3 key findings →
Participants: 85 Evidence: low
Full summary, score breakdown and related studies → Original source
The Aβ 42 /Aβ 40 ratio in the cerebrospinal fluid (CSF) and the concentrations of neurofilament light (NfL) and total tau (t-tau) are changed in the early stages of Alzheimer's disease (AD) 1 , but their neurobiological correlates are not entirely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insufficient amyloid marker test repeatability may result either from imperfection of the used laboratorial techniques or inadequate selection of control groups with their comorbidities. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β(Aβ) peptides are important components of plaques in Alzheimer's disease(AD). 2 key findings →
Participants: 588 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study confirms strong concordance between CSF biomarkers and PET Aβ-amyloid status is independent of immunoassay platform, supporting their utility as biomarkers in clinical practice for the diagnosis of AD and for participant enrichment in clinical trials. 1 key finding →
Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) studies in cognitively normal (CN) older adults age≥65 suggest depression is associated with molecular biomarkers (imaging and cerebrospinal fluid [CSF]). 2 key findings →
Participants: 248 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) positivity is defined using different biomarkers and different criteria. 3 key findings →
Participants: 368 Evidence: low
Full summary, score breakdown and related studies → Original source
Differences observed in technical and diagnostic performance of the two assays may depend on matrix-specific amyloid processing, suggesting that further studies should be carried to standardize amyloid ratio measurement in plasma. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers have been considered as a promising method for the diagnosis of Alzheimer's disease (AD). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We aimed to investigate the association of subjective sleep characteristics and plasma Alzheimer's disease (AD) biomarkers in older cognitively unimpaired adults with higher amyloid-β (Aβ) burden. 3 key findings →
Participants: 335 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that a simple blood-based signature not only provides estimates of NAB but also predicts cognitive decline and disease progression, identifying individuals at risk of progressing toward AD at the prodromal and preclinical stages. 4 key findings →
Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma amyloid beta (Aβ) and tau are emerging as accessible biomarkers for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
More than 16 million Americans living with cognitive impairment warrant a diagnostic evaluation to determine the cause of this disorder. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results show significant differences in neurogranin and total-tau between typical and atypical patients, which may relate to factors other than disease topography. 4 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We hypothesize the population without dementia can be subdivided into participants with and without biological Alzheimer disease (AD) based on the combination of CSF Aβ42 and p-tau/t-tau (represented also by the p-tau/t-tau/Aβ42 ratio). 5 key findings →
Participants: 547 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,322 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 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.
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 →