28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Viral genomes encode viral transcriptional regulators (vTRs) that manipulate host gene expression to facilitate replication and evade immune detection. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer Disease (AD) is a highly polygenic dementia that presents with relatively earlier onset (≤65yo; EOAD) in about 5% of cases. 2 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To evaluate the possible causality between Alzheimer disease (AD) and delirium, a two-sample Mendelian randomization (MR) method and gene colocalization strategy were employed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) and related dementias (ADRD) are neurodegenerative conditions that cause gradual deterioration of cognition, memory and language in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found cortical regions where a reduced glucose metabolism was maximally correlated with distributed patterns of tau, accounting for the effect of Aβ and APOE ε4 genotype. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
M07-TFN showed higher binding affinities and stronger activation of hTREM2 signaling than all previously described anti-hTREM2 antibodies. p-Syk activation was increased 30-fold in hTREM2-overexpressing HEK293 cells and fourfold in human microglia cells compared to baseline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent neurodegenerative disease associated with accumulation of amyloid beta peptides and intracellular neurofibrillary tangles formed by hyperphosphorylated Tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component. 4 key findings →
Design: case-control study Participants: 98 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study replicated the associations of SORL1, CR1, ADAM17, RASGEF1C, SPI1 , and ADAMTS1 with AD risk and protection are found in Cuban Americans. 4 key findings →
Participants: 239 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cytoplasmic mislocalisation and nuclear depletion of TDP-43 are pathological hallmarks of amyotrophic lateral sclerosis (ALS), including mutations in the C9ORF72 gene that characterise the most common genetic form of ALS (C9ALS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Treatment outcomes in the DIADS-2 trial were not significantly influenced by genetic variation at the loci that were assessed. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our results demonstrate that gene expression in trisomy 21 affected placentas significantly differs from that of chromosomally normal placentas, and this difference is only partially explained by over-expression of genes from chromosome 21. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are resident mononuclear phagocytes that play a principal role in the maintenance of normal tissue homeostasis in the central nervous system (CNS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
-weighted magnetic resonance images of 41,708 cognitively normal adults in the UK Biobank. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) polygenic risk scores (ADPRS) built from cell-type (ct) specific genetic variants can be used to infer cell-type contributions to AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the main cause of dementia and accounts for 60% of dementia syndromes in people older than 75 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We show that CD33M ectodomain dimerizes, enabling binding of large multi-sialylated molecules. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In UKB, PRS cancer was nominally associated with improved fluid intelligence ( β : 0.12, 95% CI: 0.01-0.22). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein ε4 allele (APOE4) is associated with decreased longevity and increased vulnerability to age-related declines and disorders across multiple systems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mineralized blood vessels (MBV) are a form of vascular pathology associated with cerebrovascular aging and neurodegeneration; however, their regional distribution and clinicopathological correlates in Alzheimer disease (AD) remain poorly characterized. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both 17αE2 and FMD independently reduced AD neuropathology in the EFAD mice, in an APOE-dependent manner. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Participants did not differ significantly based on sex. 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases (NDs) are common chronic diseases with unknown etiology, and the association between virus and its pathogenesis is not clear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BPSD severity was independent from cognitive impairment, vascular impairment, white matter lesions and ApoE status. 3 key findings →
Design: cross-sectional Participants: 92 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 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 →