29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Presenilin-2 (PSEN2) mutation Thr421Met was identified from a 57-years old patient with early onset Alzheimer's disease (EOAD) for the first time in Korea. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early-onset Alzheimer’s disease (EOAD) is characterized by the presence of neurological symptoms in patients with Alzheimer’s disease (AD) before 65 years of age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors describe a novel missense mutation in the presenilin 2 (PSEN2) gene at residue 439 that predicts an aspartate-to-alanine substitution (D439A). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A splice mutation (p.S290C) in PSEN1 and a missense mutation (p.V717I) in APP were identified. 2 key findings →
Participants: 67 Evidence: low
Full summary, score breakdown and related studies → Original source
A familial case of a rare autosomal dominant Alzheimer's disease (AD), related to PSEN1 gene (AD3, OMIM 607822), differing from common multifactorial form by earlier onset and, in part of cases, by accompanying neurological signs, spastic paraparesis particularly, is presented. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors describe a 28-year-old woman with histopathologically confirmed early onset Alzheimer disease characterized by severe frontal lobe involvement associated with a de novo mutation in the presenilin 1 gene (PSEN1). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) pathology has been increasingly explored through single-cell and single-nucleus RNA-sequencing (scRNA-seq & snRNA-seq) and spatial transcriptomics (ST). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of Alzheimer's disease (AD) depends on environmental and heritable factors, with its molecular etiology still unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exercise's protective effects in Alzheimer's disease (AD) are well recognized, but cell-specific contributions to this phenomenon remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The emergence of single nucleus RNA sequencing (snRNA-seq) offers to revolutionize the study of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The same vulnerable inhibitory neuron subtype was depleted in both AD and DLB. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Positron Emission Tomography (PET) ligands have advanced Alzheimer's disease (AD) diagnosis and treatment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For 50-59 greater medial temporal atrophy and flortaucipir uptake was observed in the typical compared with atypical phenotype. 5 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
We and others have shown that [18F]-Flortaucipir, the most validated tau PET tracer thus far, binds with strong affinity to tau aggregates in Alzheimer's (AD) but has relatively low affinity for tau aggregates in non-AD tauopathies and exhibits off-target binding to neuromelanin- and melanin-containing cells, and to hemorrhages. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A strong linear relationship was observed between CTR values across brain regions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found no significant changes in substantia nigra or cortex flortaucipir uptake in Parkinson's disease patients over two years and no association with changes in cognitive symptoms. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Neocortical tracer retention was highly comparable using both SUVR and distribution volume ratio-1 values obtained from dynamic scans. 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is defined by the presence of β-amyloid plaques and neurofibrillary tau tangles potentially preceding clinical symptoms by many years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
17 out of 33 patients were scored as FBB-PET positive. 5 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
Visual assessment and semiquantitative analysis provide highly congruent results, thereby enhancing reader confidence and improving scan interpretation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Within each tracer, GMM-derived amyloid negative (A-) CL distributions were similar across cohorts. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Forty-four consecutive patients with clinical evidence of dementia, were retrospectively evaluated. 5 key findings →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source
One hundred sixteen participants (Aβ- cognitively normal [CN], n = 35; Aβ- aMCI, n = 42; Aβ+ aMCI, n = 39) were included. 5 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
Among the 12 patients with PPA syndrome, 8 (66.7%) were considered as amyloid positive. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dual-phase amyloid PET is considered a useful protocol to study patients with cognitive impairment. 5 key findings →
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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 (3.5% 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 →