28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The effect of austerity and associated budgets are strong contenders,3Ruckert A Labonté R Health inequities in the age of austerity: the need for social protection policies. 3 key findings →
Evidence: low
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These preliminary findings reveal white matter alterations associated with consensus MCI diagnosis and to socioeconomic differences in a clinical cohort of rural‐dwelling older adults. 5 key findings →
Participants: 69 Evidence: moderate
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Medicaid-funded long-term services and supports (LTSS) are foundational in helping older dual-enrollees with disabilities remain in the community. 2 key findings →
Participants: 462 Evidence: low
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Our findings suggest differences in local cortical organization by neighborhood disadvantage, which also mediated the relationship between ADI and cognitive performance, providing a possible network‐based mechanism, explaining risk for cognitive decline and dementia associated with disadvantaged neighborhoods. 3 key findings →
Participants: 526 Evidence: low
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Our findings suggest differences in local cortical organization by neighborhood disadvantage, which also mediated the relationship between ADI and cognitive performance, providing a possible network‐based mechanism, explaining risk for cognitive decline and dementia associated with disadvantaged neighborhoods. 3 key findings →
Participants: 526 Evidence: low
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The study sample was NHATS respondents who needed assistance with activities of daily living (ADL) or instrumental activities of daily living (IADL), and who did not live with a spouse (N = 512). 3 key findings →
Participants: 512 Evidence: low
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Neighborhood disadvantage in later life is associated with poorer cognition and increased vulnerability to dementia. 2 key findings →
Evidence: low
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Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
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Here the current and emerging roles of brain positron emission tomography (PET) in Alzheimer's disease (AD) in the era of anti-amyloid-β antibody therapy, with a focus on clinical applications, methodological considerations, and future perspectives were reviewed. 5 key findings →
Design: narrative review Evidence: low
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Recent advances in Blood-Based Biomarkers (BBMs) are transforming the diagnostic landscape of Alzheimer Disease (AD), with plasma p-tau217 emerging as a highly accurate and scalable diagnostic marker of AD pathology. 2 key findings →
Evidence: low
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P. gingivalis-induced periodontitis dampened hippocampal Bmal1 rhythms, lowered p-AKT, activated glia, and elevated Aβ and interleukin 1β (IL-1β). 4 key findings →
Evidence: low
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A doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva cuja fisiopatologia envolve, entre outros mecanismos, o acúmulo cerebral de β-amiloide, associado a alterações da proteína tau, sua hiperfosforilação e formação de emaranhados neurofibrilares, contribuindo para a disfunção sináptica e a perda neuronal. 5 key findings →
Design: longitudinal study Evidence: moderate
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Among 1,706 participants (mean age 56 years, 62% female, 28% Black), midlife NAFLD vs no NAFLD was associated with greater late-life WMH volume (difference per SD 0.19, 95% CI 0.06-0.31) and faster late-life WMH increase over 6 years (difference in annual change, SD 0.28, 95% CI 0.05-0.51), suggesting accumulating vascular pathology. 5 key findings →
Participants: 1,706 Evidence: low
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In the whole sample, both PRSs were associated with the strength of correlation between GMV and different serotonin receptors and fluorodopa uptake. 2 key findings →
Evidence: low
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Research revealed a significant locus of susceptibility for LOAD on the Bridging Integrator 1 (BIN1) that is situated on chromosome 2q14.3 and is identified at the time of the most significant susceptibility gene of LOAD. 2 key findings →
Participants: 110 Evidence: low
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Genome-wide association studies (GWASs) have identified thousands of putative disease-causing variants with unknown regulatory effects. 1 key finding →
Evidence: low
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Epidemiological evidence suggests an association between celiac disease (CeD) and Alzheimer disease (AD). 3 key findings →
Evidence: low
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Within the limitations of measuring in vitro equilibrium binding activity of in‐house recombinant antibodies to aqueously extracted Aβ from human postmortem brain tissue, we could not discern a population of Aβ aggregates ( e.g . protofibrils) accessible to one antibody but not the other two. 3 key findings →
Evidence: low
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Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood. 1 key finding →
Evidence: low
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The anti-amyloid monoclonal antibody lecanemab received the US accelerated approval for mild cognitive impairment or mild dementia stage of Alzheimer disease in January 2023, which was converted into traditional approval in June 2023. 5 key findings →
Evidence: low
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Our results show that lecanemab exhibits high binding affinity to amyloid-β fibril structures that have a flexible N-terminus in common, as is the case for type I, type II and murine type III amyloid-β fibril polymorphs, which resemble or are identical to human structures observed in sporadic and familial cases of Alzheimer's disease, including a case with the Arctic (E22G) mutation. 5 key findings →
Evidence: low
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Lecanemab reduced clinical decline by roughly 27% over placebo, with ARIA-E in 12.6% of treated patients;donanemab slowed decline by about 35%, with ARIA-E near 24%. 4 key findings →
Design: narrative review Evidence: high
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-glycans found at the N304 site of lecanemab of the heavy chain. 1 key finding →
Evidence: low
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Evidence: low
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Alzheimer's disease (AD) affects ~55 million people globally and is projected to rise steeply with population ageing. 1 key finding →
Design: longitudinal study Evidence: moderate
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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 →