27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Positive cerebrospinal fluid (CSF) biomarkers of tau and amyloid beta42 suggest possible active underlying Alzheimer's disease (AD) including neurometabolic dysfunction and neurodegeneration leading to eventual cognitive decline. 4 key findings →
Design: cohort study Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Brain amyloid-beta (Aβ) plaques, a hallmark of the pathophysiology of Alzheimer's disease, have been associated with frailty. 4 key findings →
Participants: 477 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The sensitivity of amyloid to pre-analytic factors complicates cerebrospinal fluid (CSF) diagnostics for Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 727 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A possible involvement of the gene IL1RAP (interleukin-1 receptor-associated protein) in the pathogenesis of Alzheimer's disease (AD) has been suggested in GWASs of cerebrospinal fluid (CSF) tau levels and longitudinal change in brain amyloid burden. 4 key findings →
Design: longitudinal study Participants: 3,446 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
It remains unknown whether the associations between protective lifestyles and sporadic dementia risk reported in observational studies also affect age at symptom onset (AAO) in autosomal dominant Alzheimer disease (ADAD) with predominant genetic influences. 4 key findings →
Design: longitudinal study Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
According to all previous literature, they are not associated with mortality. 4 key findings →
Participants: 456 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Loss-of-function mutations in the GBA gene are associated with more severe cognitive impairment in PD, but the nature of these deficits is not well understood and whether common GBA polymorphisms influence cognitive performance in PD is not yet known. 4 key findings →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
135 subjects enrolled in a longitudinal clinicopathologic study were administered the MoCA by a single physician and the MMSE by a trained research assistant. 4 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study was designed to evaluate whether subjects with amyloid beta (Aβ) pathology, detected using florbetapir positron emission tomorgraphy (PET), demonstrated greater cognitive decline than subjects without Aβ pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma sphingolipids have been shown to predict cognitive impairment and hippocampal volume loss, but there is little research in patients with Alzheimer's disease (AD). 4 key findings →
Design: cross-sectional Participants: 120 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia with Lewy bodies (DLB) needs to be distinguished from Alzheimer's disease (AD) because of important differences in patient management and outcome. 4 key findings →
Participants: 61 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is evidence that major depression increases the risk for dementia, but there is conflicting evidence as to whether depression may accelerate cognitive decline in dementia. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A high intake of saturated fat and cholesterol and a low intake of polyunsaturated fatty acids have been related to an increased risk of cardiovascular disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer's Disease Neuroimaging Initiative (ADNI) measures abilities broadly related to executive function (EF), including WAIS-R Digit Symbol Substitution, Digit Span Backwards, Trails A and B, Category Fluency, and Clock Drawing. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Four subtypes emerged: (1) dysnomic (n = 153), (2) dysexecutive (n = 102), (3) amnestic (n = 288), and (4) cluster-derived normal (n = 282) who performed within normal limits on cognitive testing. 4 key findings →
Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sleep disturbance is common in dementia, although it is unclear whether differences in sleep architecture precede dementia onset. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The American Heart Association developed the ideal cardiovascular health (CVH) index as a simple tool to promote CVH; yet, its association with brain atrophy and dementia remains unexamined. 4 key findings →
Participants: 2,750 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cardiometabolic diseases (hypertension, coronary artery disease [CAD] and diabetes are known to associate with poorer cognitive ability but there are limited data on whether having more than one of these conditions is associated with additive effects. 4 key findings →
Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Air pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. 4 key findings →
Participants: 680 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The CDR® plus NACC FTLD was able to detect early symptoms in the mildly impaired participants who were rated as CDR® sum of boxes (CDR®-SB) = 0. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Even before dementia becomes apparent, cognitive decline may contribute to deterioration in oral health. 4 key findings →
Design: cohort study Participants: 10,050 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study formed part of the Rotterdam Study, a prospective, population-based cohort study on the frequency, etiology, and prognosis of chronic diseases. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cysteine-altering NOTCH3 variants identical to those causing the rare monogenic form of stroke, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), have been reported more common than expected in the general population, but their clinical significance and contribution to stroke and dementia risk in the community remain unclear. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 →