27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aggregation of the microtubule-stabilizing protein Tau into insoluble deposits is characteristic for several neurodegenerative diseases, including Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD), the most common neurodegenerative disease in the world, is caused by a variety of factors that lead to neuronal injury and an alteration in neurotransmitter production and release. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks. 3 key findings →
Design: clinical trial Participants: 370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structural studies of amyloid fibrils extracted from brain tissue have identified disease-specific fibril polymorphs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid-β (Aβ) immunotherapy improves cognitive outcomes in Alzheimer’s disease (AD) but is associated with amyloid-related imaging abnormalities (ARIA), through poorly understood mechanisms. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ42 rose from 526.0 to 1053.0 pg/mL (+ 100.2%), total tau (t-tau) fell from 578.2 to 278.0 pg/mL(-51.9%), and phosphorylated tau181 (p-tau181) fell from 90.8 to 23.1 pg/mL(-74.6%). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease disrupts large-scale brain networks before cognitive symptoms emerge, yet the mechanisms underlying this progression remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From 464 identified records, 30 peer-reviewed primary studies met all eligibility criteria following the exclusion of low-quality sources and unindexed preprints. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Amyloid plaques, one of the defining features of Alzheimer’s disease, are associated with synapse loss and accumulation of pathological tau in dystrophic neurites and reactive glia in their immediate vicinity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Artificial intelligence (AI) is now a credible translational research platform across the Alzheimer’s disease (AD) pathway, but its clinical value is often difficult to judge from performance metrics alone. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The cost-effectiveness of ATTs is strongly influenced by the waning of the treatment effect. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
A major obstacle to effective Alzheimer’s disease therapy is the limited ability to deliver therapeutics across the blood-brain barrier. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Distinct PTMs delineate the compartment-specific architectural signatures of Aβ deposits. 2 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
The overall incidence of any ARIA was 25.2%, with ARIA-H occurring in 22.4% of patients and ARIA-E in 12.2%. 3 key findings →
Design: cohort study Participants: 468 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MCH-Guard offers a flexible clinical decision-support tool for optimizing spontaneous MCH & ARIA surveillance. 1 key finding →
Design: longitudinal study Participants: 813 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Temporal imaging variables may provide independent prognostic information beyond baseline risk, supporting a dynamic model of haemorrhagic risk in Alzheimer’s disease. 2 key findings →
Participants: 1,069 Evidence: low
Full summary, score breakdown and related studies → Original source
We trained a self-configuring nnU-Net model for CMB segmentation in a hetero-geneous multicenter sample ( n =264), including 1.5T and 3T field strengths, SWI and T2*-GRE sequences, and community and clinical cohorts. 1 key finding →
Participants: 264 Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-Aβ immunotherapies for Alzheimer’s Disease (AD) have high rates of amyloid-related imaging abnormalities (ARIA), an adverse side effect with markedly higher rates in APOE4 carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Under calibrated simulation parameters, slowing of cognitive decline emerged as the most important attribute (relative importance 25.7%), followed by annual cost (17.6%), ARIA risk (15.4%), and travel to treatment centre (13.0%). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Simulation-based validation demonstrates the framework’s analytical capability. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses. 3 key findings →
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →