30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We found MTL neurodegeneration largely consistent with existing models, suggesting that harmonized MRI volumetry may be used under conditions that are common in clinical multi-center cohorts. 5 key findings →
Design: longitudinal study Participants: 206 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These data suggest that apoJ may have potential in the context of use (COU) of AD diagnostics, I-309 may be specifically useful in the COU of identifying individuals at greatest risk for progressing toward AD. 2 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In conjunction with the NILVAD trial, a European Multicentre Double-Blind Placebo Controlled trial of Nilvadipine in Mild-to-Moderate Alzheimer's disease (AD), there are four NILVAD substudies in which eligible NILVAD patients are also invited to participate. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
JOURNAL/nrgr/04.03/01300535-202508000-00027/figure1/v/2024-09-30T120553Z/r/image-tiff Several promising plasma biomarker proteins, such as amyloid-β (Aβ), tau, neurofilament light chain, and glial fibrillary acidic protein, are widely used for the diagnosis of neurodegenerative diseases. 2 key findings →
Design: cohort study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Digital biomarkers are defined as objective, quantifiable physiological and behavioral data that are collected and measured by means of digital devices. 4 key findings →
Design: longitudinal study Participants: 568 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Numerous studies have found associations between characteristics of urban environments and risk factors for dementia and cognitive decline, such as physical inactivity and obesity. 1 key finding →
Design: cohort study Participants: 1,800 Evidence: moderate
Full summary, score breakdown and related studies → Original source
TBCA has emerged to solve the limitations of administering cognitive assessments face-to-face. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
These findings support the use of the NIHTB-CB in early AD, but also imply that the optimal NIHTB-CB composite score to detect change over time may differ across clinical stages of AD. 3 key findings →
Design: cross-sectional Participants: 171 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results suggest that a longitudinal digital biomarker differentiates between controls and patients with MCI in a very cost-effective and noninvasive way and hence may be very useful for identifying patients with very early AD who can benefit from clinical trials and new, disease-modifying therapies. 3 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increased cardiovascular risk as evidenced by FRS was associated with poorer cognitive performance in all cognitive domains among dementia-free middle-aged and older rural Indians. 3 key findings →
Design: cross-sectional Participants: 3,609 Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE e4 genotype prevalence varies among AD patients by region and within each country. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Hippocampal sclerosis pathology can be associated with different underlying causes, and we refer to hippocampal sclerosis in the aged brain as hippocampal sclerosis associated with ageing. 5 key findings →
Design: longitudinal study Participants: 106 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) 42 amino acid species of amyloid beta (Aβ42) and tau levels are strongly correlated with the presence of Alzheimer's disease (AD) neuropathology including amyloid plaques and neurodegeneration and have been successfully used as endophenotypes for genetic studies of AD. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We identified common genetic variants in C9orf72, but in addition in UNC13A that are shared between ALS and FTD. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Providing ostensibly healthy individuals with personal results from whole-genome sequencing could lead to improved health and well-being via enhanced disease risk prediction, prevention, and diagnosis, but also poses practical and ethical challenges. 5 key findings →
Design: cohort study Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma proteins derived from specific organs can estimate organ age and mortality, but their sensitivity to environmental factors and their robustness in forecasting onset of organ diseases and mortality remain unclear. 3 key findings →
Participants: 44,498 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular risks interact with subthreshold levels of Aβ to promote cognitive decline, partially by accelerating early neocortical tau accumulation. 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
However, these abnormal levels do not appear to be the result of a high rate of accumulation in the short term, but possibly a more moderate rate occurring early with respect to age. 1 key finding →
Design: longitudinal study Participants: 447 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings offer novel perspectives to the design of AD clinical trials and aid in understanding the tau accumulation inside and outside MTL in AD. 5 key findings →
Design: longitudinal study Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BIN1-associated AD risk is potentially driven by accelerated tau accumulation in the face of Aβ. 4 key findings →
Design: longitudinal study Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deposition of amyloid and tau pathology can be quantified in vivo using positron emission tomography (PET). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Since tau PET tracers were introduced, investigators have quantified them using a wide variety of automated methods. 1 key finding →
Design: cohort study Participants: 415 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared with Aβ-negative persons, those with regional Aβ binding showed proportionately more APOE ε4 carriers (18 [64%] vs 22 [27%] in PREVENT-AD and 34 [31%] vs 38 [19%] in ADNI), reduced CSF Aβ1-42 levels (F = 24 and 71), and greater longitudinal Aβ-PET accumulation (significant β = 0.019 to 0.056). 3 key findings →
Design: cohort study Participants: 817 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In older adults, longitudinal hippocampal atrophy is associated with cognitive decline, independently of Aβ or tau, suggesting that non-AD pathologies (e.g., TDP-43, vascular) may contribute to hippocampal-mediated cognitive decline. 4 key findings →
Design: cohort study Participants: 283 Evidence: moderate
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →