27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
[ 18 F]Tauvid and [ 18 F]MK6240 capture largely overlapping patterns of tau pathology, but differ notably in the magnitude of off-target binding. 3 key findings →
Participants: 681 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain positron emission tomography (PET) imaging is a valuable tool which allows visualization of the pathological structures inside the living patients’ brains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
PVeD reproducibly contextualized associations between plasma pTau217 and PET-defined Alzheimer pathology across cohorts with different participant composition, pTau217 assays, PET tracers, and cognitive measures. 2 key findings →
Participants: 602 Evidence: low
Full summary, score breakdown and related studies → Original source
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid-β and tau, pathological hallmarks of AD, silently accumulate years before clinical symptoms’ onset and are associated with neuronal dysfunction and cognitive impairment. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain perfusion SPECT revealed AD-typical hypoperfusion patterns and demonstrated modest potential to estimate the presence or absence of Aβ deposition with left parietal rCBF. 5 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology develops years in advance prior to its clinical presentation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study investigated whether WM measures derived from amyloid-PET are associated with AD biomarkers and to determine whether they offer added diagnostic and prognostic value beyond established biomarkers. 5 key findings →
Participants: 320 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease and cerebral amyloid angiopathy are characterized by the accumulation of amyloid-β (Aβ) species, yet the human fluid-physiological mechanisms that regulate soluble Aβ transport and clearance remain poorly understood. 3 key findings →
Participants: 502 Evidence: moderate
Full summary, score breakdown and related studies → Original source
As the world's population ages, Alzheimer's disease (AD), a progressive neurodegenerative disorder, is becoming more common. 1 key finding →
Participants: 59 Evidence: low
Full summary, score breakdown and related studies → Original source
Under nested cross-validation, the WWL kernel achieves a balanced accuracy of $0.651\pm0.028$, significantly outperforming both a raw-feature SVM and a histogram-based WL-kernel baseline. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder, and early diagnosis is essential for timely intervention. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate differential diagnosis between Alzheimer’s disease (AD) and frontotemporal dementia (FTD) is of critical importance for the early screening of neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s Disease (AD) changes how the brain’s electrical activity behaves, and these changes can, in principle, be picked up directly from a resting-state EEG recording without any invasive testing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Resting-state EEG is a scalable modality for neurophysiological screening, but conventional spectral descriptors capture only part of the signal organization altered in neurodegenerative disease. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
The disorders fell into one of three categories based on the topographic relationship of the disease-specific and healthy networks. 5 key findings →
Participants: 1,117 Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disturbances are pervasive in Lewy body disorders (LBD), but their neurophysiological basis remains unclear. 1 key finding →
Participants: 109 Evidence: low
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 27,380 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 →