This ITR analysis provides a proof of concept for precision medicine in future AD research and drug development. 3 key findings →
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 provide evidence that greater concentrations of KP metabolites are associated longitudinally over two years with greater biomarker evidence of neurofibrillary tau pathology (pTau-181), neuroinflammation (GFAP), and neurodegeneration (NfL), suggesting that dysregulated KP metabolism may play a role in ADRD pathogenesis. 4 key findings →
Participants: 301 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma BD-tau is a valuable marker for CJD prognostication. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Men and women with MCI may to differ for which factors predict subsequent dementia although future analyses with greater power are needed to evaluate sex differences. 5 key findings →
Participants: 449 Evidence: low
Full summary, score breakdown and related studies → Original source
Lobar distribution of cerebral microbleeds is associated with Alzheimer's disease and the number of lobar cerebral microbleeds directly correlates with cerebrospinal fluid amyloid-beta and phosphorylated tau 181 protein levels and with the cognitive decline of Alzheimer's disease patients. 2 key findings →
Participants: 54 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers for Alzheimer's disease (AD), such as plasma phosphorylated (p)-tau217, offer a more accessible means of testing for the presence of AD pathology compared to cerebrospinal fluid (CSF) or positron emission tomography (PET) methods. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic loss strongly correlates with cognitive impairment in Alzheimer's disease (AD), yet the mechanism linking its origin and pattern remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Differences in the stability of Aβ42 and p-tau217 may lead to altered p-tau217/Aβ42 ratio results if samples are not handled properly during the pre-analytical testing phase. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Our study revealed the possibility of urinary formic acid as a potential novel biomarker for the early diagnosis of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive irreversible neurodegenerative disorder that represents a major global public health concern. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This nFC-based assay accurately distinguishes MCI and AD plasma without EV isolation, offering a rapid approach requiring minute sample volumes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and vascular dementia (VaD) are intertwined by mixed dementia (MD) harboring varying degrees of AD pathology in combination with cerebrovascular disease. 5 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicate that neuroinflammation is linked to the symptomatic phase of ALS/FTD and shows a similar pattern in sporadic and genetic cases. 3 key findings →
Participants: 16 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
48/100
Reduced neurogenesis in the aging mammalian hippocampus has been linked to cognitive deficits and increased risk of dementia. 3 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
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
48/100
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
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 →