30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Data-driven WMH spatial patterns reflect discrete underlying etiologies including arteriolosclerosis, CAA, AD, and normal aging. 4 key findings →
Design: cross-sectional Evidence: low
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Accounting for educationalfactors, vascular factors, and Aβ burden diminished, but did not eliminate, racial differences in PACC5 performance longitudinally. 4 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
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The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients. 1 key finding →
Participants: 497 Evidence: low
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Longitudinal racial differences in amyloid biomarkers are observed. 1 key finding →
Design: longitudinal study Participants: 179 Evidence: moderate
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These findings suggest EPVS burden to be a potential marker of both CSVD and AD-related BBM pathology. 3 key findings →
Design: cross-sectional Participants: 979 Evidence: moderate
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Although there were no significant differences among the 3 groups of participants in their clinical ratings, neuropsychological test scores, hippocampal volumes (P = .60), or hippocampal glucose metabolism measurements (P = .12), there were significant group differences in their posterior cingulate glucose metabolism measurements (P = .001). 2 key findings →
Design: cross-sectional Participants: 31 Evidence: low
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The impact of APOE4 on brain metabolism and structure is modified by sex. 3 key findings →
Design: cross-sectional Participants: 274 Evidence: low
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These results indicate that trans-resveratrol has potential neuroprotective roles in the treatment of moderate to mild AD and that its mechanism may involve a reduction in the accumulation and toxicity of Aβ in the brain of patients, thereby reducing neuroinflammation. 4 key findings →
Design: case-control study Participants: 15 Evidence: moderate
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Individuals with an isolated pathologic diagnosis of AD, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle--only degeneration usually had substantial hippocampal atrophy, while those with changes of typical aging did not. 2 key findings →
Participants: 67 Evidence: low
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Circulating leptin was associated with a reduced incidence of dementia and AD and with cerebral brain volume in asymptomatic older adults. 4 key findings →
Participants: 785 Evidence: moderate
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Whole brain atrophy rate discriminates Alzheimer disease (AD) from MCI. 1 key finding →
Participants: 64 Evidence: low
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ALPS-index may provide useful disease progression or treatment biomarkers for patients with AD as an indicator of modulation of glymphatic activity. 1 key finding →
Participants: 50 Evidence: low
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Accumulating white matter changes in advanced age are likely driven by small-vessel ischemic disease. 4 key findings →
Design: longitudinal study Evidence: moderate
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CA1 apical neuropil atrophy is apparent in patients with mild AD. 2 key findings →
Design: cross-sectional Participants: 14 Evidence: low
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MeDi groups were comparable for clinical and neuropsychological measures. 2 key findings →
Participants: 34 Evidence: low
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In our study, TSH was related neither to risk of AD nor with early MRI markers thereof, arguing against an important role of thyroid function in the development of AD. 4 key findings →
Design: cohort study Participants: 1,025 Evidence: moderate
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Three women (aged 61, 72, and 73 years) consecutively enrolled in the trial successfully completed repeated focused ultrasound-induced BBB opening of the hippocampus and entorhinal cortex. 1 key finding →
Evidence: low
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life. 2 key findings →
Design: cross-sectional Participants: 138 Evidence: low
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Although white matter hyperintensities have traditionally been viewed as a marker of vascular disease, recent pathology studies have found an association between white matter hyperintensities and Alzheimer's disease pathologies. 4 key findings →
Participants: 434 Evidence: low
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Clinical data alone poorly predicted phenoconversion in RBD due to synucleinopathy patients. 3 key findings →
Participants: 173 Evidence: low
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In idiopathic normal pressure hydrocephalus, we found delayed enhancement (P < 0.05) and decreased clearance of gadobutrol (P < 0.05) at the Sylvian fissure. 1 key finding →
Evidence: low
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Empathy is a complex social behaviour mediated by a network of brain structures. 3 key findings →
Participants: 123 Evidence: low
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To design clinical trials for the frontotemporal lobar degenerations (FTLD), knowledge about measurement of disease progression is needed to estimate power and enable the choice of optimal outcome measures. 2 key findings →
Participants: 107 Evidence: low
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Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769 Evidence: low
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Accurate prediction of clinical changes of mild cognitive impairment (MCI) patients, including both qualitative change (i.e., conversion to Alzheimer's disease (AD)) and quantitative change (i.e., cognitive scores) at future time points, is important for early diagnosis of AD and for monitoring the disease progression. 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.
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →