27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 132 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A mortality risk score derived from MDS data predicted six-month survival in advanced dementia with moderate accuracy. 1 key finding →
Design: cohort study Participants: 22,405 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hospice enrollment correlates with reduced Medicare expenditures among younger decedents with cancer but increased expenditures among decedents without cancer and those older than 84 years of age. 2 key findings →
Design: retrospective cohort Participants: 245 Evidence: moderate
Full summary, score breakdown and related studies → Original source
NHs appear to provide less-aggressive end-of-life care to decedents with dementia than to those without. 4 key findings →
Design: longitudinal study Participants: 1,261,726 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Extrapolating results to the US population, we estimate that annually nearly a million individuals who are likely eligible for hospice die without its services. 4 key findings →
Design: cohort study Participants: 1,209 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results demonstrate delirium is a significant marker of mortality among seniors in the ED, and mortality risk is most salient in the first 3 months following an ED visit. 5 key findings →
Design: cohort study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Real-world deprescribing patterns of antihypertensives among NH residents with HTN and LLE/AD appear to reflect variation in recommendations for HTN treatment intensity and individualization of patient care in a population with potential overtreatment. 5 key findings →
Design: cohort study Participants: 10,574 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Later GOCDs were associated with greater risk of aggressive interventions and death as an inpatient and greater odds of ICU admission. 3 key findings →
Design: cohort study Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Palliative care is related to reduced life-sustaining treatments for patients with dementia. 3 key findings →
Design: cohort study Participants: 1,996 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Twenty-seven (27.3%) of the 99 women developed incident dementia. 5 key findings →
Design: longitudinal study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Diabetes and prediabetes accelerate cognitive decline and might predict microvascular lesions among dementia-free older adults. 4 key findings →
Design: longitudinal study Participants: 2,746 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive impairment short of dementia affects nearly one in four community-dwelling elders and is a major risk factor for later development of dementia. 1 key finding →
Design: longitudinal study Participants: 351 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Incident AF was associated with an increased risk of dementia, independent of clinical stroke in an elderly population. 5 key findings →
Design: longitudinal study Participants: 435 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An increasing number of cardiometabolic diseases was dose-dependently associated with the decline in cognitive function score (one disease, β=-0·15 [95% CI -0·17 to -0·13]; two diseases, β=-0·37 [-0·40 to -0·34]; three diseases, β=-0·57 [-0·64 to -0·50]), with comorbid diabetes and stroke (β=-0·23 [-0·29 to -0·17]) contributing most strongly to cardiometabolic disease-associated cognitive decline. 3 key findings →
Design: cohort study Participants: 147 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. 2 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This large study shows the role of plasma biomarkers in differentiating patients with different dementias, and at monitoring longitudinal change. 5 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →
Design: longitudinal study Participants: 199 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study confirms the role of NFL as a biomarker in ALS. 3 key findings →
Design: longitudinal study Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We believe that ours is the largest blood biomarker study of preclinical AD to date. 3 key findings →
Design: longitudinal study Participants: 28 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma markers can track biological change over time, with plasma pTau181 and GFAP markers showing longitudinal change in individuals with preclinical AD. 3 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of PRSs may be beneficial for increased precision in risk estimates among APOE4 carriers. 3 key findings →
Design: cohort study Participants: 712 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Conventional neuropsychological assessments for Alzheimer's disease are burdensome and inaccurate at detecting mild cognitive impairment and predicting Alzheimer's disease risk. 3 key findings →
Design: longitudinal study Participants: 525 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We initiated the systematic profiling of the dorsolateral prefrontal cortex obtained from a subset of autopsied individuals enrolled in the Religious Orders Study (ROS) or the Rush Memory and Aging Project (MAP), which are jointly designed prospective studies of aging and dementia with detailed, longitudinal cognitive phenotyping during life and a quantitative, structured neuropathologic examination after death. 5 key findings →
Design: longitudinal study Participants: 2,090 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We undertook a genome-wide association study (GWAS) of parental longevity in European descent UK Biobank participants. 4 key findings →
Design: longitudinal study Participants: 1,181 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →