28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Functional phenotypes (e.g., subcortical surface representation), which commonly arise in imaging genetic studies, have been used to detect putative genes for complexly inherited neuropsychiatric and neurodegenerative disorders. 2 key findings →
Participants: 708 Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical models of Alzheimer's disease (AD) suggest APOE modulates brain function in structures vulnerable to AD pathophysiology. 5 key findings →
Participants: 608 Evidence: low
Full summary, score breakdown and related studies → Original source
Gene-based PRS identified 389 genes with 164 of them not previously reported as AD-associated. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain iron accumulation, which is indicated in the cerebrospinal fluid (CSF) ferritin, is associated with the development of Alzheimer's Disease (AD). 4 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has multiple clinically and pathologically defined subtypes where the underlying causes of such heterogeneity are not well established. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a novel mutation c.401_406delinsTCTAT; p.(Asp134Valfs*55) in exon 3 of TREM2 in an Alzheimer's disease patient also carrying the p.Arg62His TREM2 variant. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a central regulator of microglial activity and loss-of-function coding variants are major risk factors for late onset Alzheimer's disease (LOAD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified a PSEN1 variant (p.Thr291Pro) in an individual presenting with pure SP at 30 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 5 key findings →
Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglia are central mediators of neuroinflammation in Alzheimer's disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia and cognitive disorders are major aging-associated pathologies. 4 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) is linked to a higher risk of premature aging, but the mechanisms underlying this association remain unclear. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although Alzheimer's disease (AD) is a central nervous system disease and type 2 diabetes MELLITUS (T2DM) is a metabolic disorder, an increasing number of genetic epidemiological studies show clear link between AD and T2DM. 5 key findings →
Participants: 448 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia with advancing age as its strongest risk factor. 3 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), trisomy of human chromosome 21 (HSA21), is characterized by lifelong cognitive impairments and the development of the neuropathological hallmarks of Alzheimer's disease (AD). 4 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
The novel tau-PET tracer [18F]PI-2620 detects the 3/4-repeat-(R)-tauopathy Alzheimer's disease (AD) and the 4R-tauopathies corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). 2 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Older participants had lower hippocampal volumes and overall flortaucipir uptake. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
18 F-Flortaucipir, as a classical Tau protein visualizer, has been widely used in the diagnosis of neurodegenerative diseases, especially Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with suspected AD neuropathology (Aβ-positive patients with mild cognitive impairment or AD dementia) showed high-intensity temporoparietal cortex-predominant [18F]PI-2620 binding. 5 key findings →
Participants: 65 Evidence: low
Full summary, score breakdown and related studies → Original source
Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are clinical syndromes that commonly have underlying Alzheimer's disease (AD), although non-AD pathologies have also been reported. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher neuroticism is a risk factor for Alzheimer's disease (AD), and is implicated in disordered stress responses. 4 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
There were significant associations (p < 0.05) between the NPI variables (total score, Affective factor) and entorhinal and precuneus tau across all participants. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Among 565 veterans, 34.9% of received an amyloid PET scan and 98.0% of these were consistent with appropriate use criteria. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The cortical SUVR (R2 = 0.97) and striatal SUVR (R2 = 0.95) demonstrated an excellent linear correlation between FBB and FMM using a WC as reference region. 5 key findings →
Participants: 107 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 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 →