28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
We investigated whether the cerebrospinal fluid (CSF) biomarkers beta-amyloid 1-42 (Abeta1-42), total tau (t-tau) protein and tau protein phosphorylated at threonine 181 (p-tau181) could discriminate Alzheimer's disease (AD) from vascular dementia (VD) patients. 4 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of epilepsy is increased among Alzheimer's Disease (AD) patients and cognitive impairment is common among people with epilepsy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings indicate that GFAP is of potential clinical utility in screening amyloid pathology and predicting future cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We underline the potential of next-generation biomarker identification tools to detect novel proteomic features that also incorporate established biomarkers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the community, the concentration of AD blood biomarkers varies in relation to medical conditions and systemic inflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The levels of plasma ATN biomarkers (Aβ42/Aβ40 ratio, p-tua181, and NfL) were significantly changed in clinically diagnosed AD patients and they all associated with different domains of cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choice of tau biomarker may differ by disease stage and research goals that seek to maximize sensitivity or specificity. 2 key findings →
Participants: 351 Evidence: low
Full summary, score breakdown and related studies → Original source
Oligomeric-Aβ mediates the maturation of tau pathology and its neuronal toxicity in macaques but not its initial spreading. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
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
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
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →