27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Both early life and adult socioeconomic status (SES) predict late-life level of memory; however, evidence is mixed on the relationship between SES and rate of memory decline. 4 key findings →
Design: longitudinal study Participants: 10,781 Evidence: moderate
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The Honolulu-Asia Aging Study is a longitudinal study of Japanese-American men living in Hawaii. 4 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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Dementia occurs in at least 10% of patients within 1 year after stroke. 4 key findings →
Design: cohort study Participants: 218 Evidence: moderate
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There is clinical overlap between presentations of dementia due to limbic-predominant age-related TDP-43 encephalopathy (LATE) and Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 78 Evidence: moderate
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The recent availability of longitudinal data on the possible association of different lifestyles with dementia and Alzheimer's disease (AD) allow some preliminary conclusions on this topic. 4 key findings →
Design: longitudinal study Evidence: moderate
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Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood. 3 key findings →
Participants: 427 Evidence: low
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We aimed to verify the association between diabetes and the risk of dementia, Alzheimer's disease, and vascular dementia in twins and to explore whether genetic and early-life environmental factors could contribute to this association. 4 key findings →
Design: case-control study Participants: 13,693 Evidence: moderate
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This longitudinal study examined whether insulin resistance among late middle-aged, cognitively healthy individuals was associated with 1) less gray matter in Alzheimer disease-sensitive brain regions and 2) worse cognitive performance. 4 key findings →
Design: longitudinal study Participants: 372 Evidence: moderate
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Synapse loss in Alzheimer's disease (AD) correlates with cognitive decline. 4 key findings →
Evidence: low
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Knowledge of the relationship between various clinical characteristics and cognitive functioning is advancing, but little is known about the cognitive response to treatment for geriatric depression. 4 key findings →
Participants: 45 Evidence: low
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Cognitive decline is a leading cause of disability and death in old age but its neurobiological bases are not well understood. 4 key findings →
Design: cohort study Participants: 130 Evidence: moderate
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The aim of this multicenter randomized controlled trial was to determine whether the incidence of dislocation one year after total hip arthroplasty is significantly lower in association with the use of a 36-mm femoral head articulation as compared with a 28-mm articulation. 4 key findings →
Design: randomized controlled trial Evidence: high
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Two (1.5%) persons met NIA-Reagan criteria for high likelihood AD, and 48 (35.8%) met criteria for intermediate likelihood; 29 (21.6%) had cerebral infarctions, and 18 (13.4%) had Lewy bodies. 5 key findings →
Participants: 2,000 Evidence: low
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Transactive response DNA-binding protein of ∼43 kDa (TDP-43), a primary pathologic substrate in tau-negative frontotemporal lobar degeneration (FTLD), is also often found in the brains of elderly individuals without FTLD and is a key player in the process of neurodegeneration in brains with and without FTLD. 4 key findings →
Design: longitudinal study Participants: 68 Evidence: moderate
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Neurodegenerative pathologies such as Alzheimer disease neuropathologic change (ADNC), Lewy body disease (LBD), limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC), and cerebrovascular disease (CVD) frequently coexist, but little is known about the exact contribution of each pathology to cognitive decline and dementia in subjects with mixed pathologies. 4 key findings →
Participants: 6,262 Evidence: moderate
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Two distinct literacy profiles emerged. The first group (N=121, 44%) had higher level of literacy at baseline, slower decline and less variabilities over time. 5 key findings →
Design: longitudinal study Participants: 121 Evidence: moderate
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CSF was αSyn-SAA positive (αSyn+) in 36/80 AD patients (45%) and in 2/28 controls (7.1%). 5 key findings →
Design: longitudinal study Evidence: moderate
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We have undertaken a large unselected, community-based neuropathology study in an elderly (70-103 years) UK population in relation to prospectively evaluated dementia status. 4 key findings →
Participants: 209 Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. 4 key findings →
Participants: 111 Evidence: low
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The neuropathologic substrate of amnestic mild cognitive impairment (aMCI) is not known. 4 key findings →
Design: cohort study Participants: 23 Evidence: moderate
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Patients with AD and individuals at risk for AD show reduced glucose metabolism, as indexed by fludeoxyglucose F 18-labeled positron emission tomography (FDG-PET). 4 key findings →
Design: cross-sectional Participants: 150 Evidence: low
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The degree to which Alzheimer's versus other neuropathologies contribute to the risk of Alzheimer's dementia is unknown. 4 key findings →
Participants: 1,161 Evidence: low
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The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention. 4 key findings →
Participants: 4,110 Evidence: moderate
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We examined the pattern of cognitive impairment and rate of cognitive and functional decline as a function of age at symptom onset in 127 patients with probable Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 127 Evidence: moderate
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Thirty percent of the cases had significant cerebrovascular parenchymal pathology scores (CVDPS), 54% had significant AD pathology, and 18% had HS. 4 key findings →
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 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 →