29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
To investigate potential associations between cerebrospinal fluid (CSF) microplastics and Alzheimer's disease (AD) pathology or cognitive function. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified numerous genetic variants associated with AD risk, while a transcriptomic analysis has revealed dysregulated gene expression patterns in the brains of individuals with AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma BD-tau and p-tau181 mimic their corresponding cerebrospinal fluid (CSF) markers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL and GFAP predict cognitive decline in a similar manner to traditional imaging techniques in amyloid-positive MCI patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Considering renal function and age is crucial when interpreting AD biomarkers in the general aging population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An improved understanding of the pathobiology of Alzheimer's disease (AD) should lead ultimately to an earlier and more accurate diagnosis of AD, providing the opportunity to intervene earlier in the disease process and to improve outcomes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers for Alzheimer's disease (AD) are a promising tool that may help in early diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicates that Aβ-induced astrocytic autophagic plasticity is an important cellular event to modulate Aβ clearance and maintain cognitive function in AD mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We demonstrated senile plaques with glial fibrillary acidic protein (GFAP) stain in prefrontal and parietal cortex and in hippocampus of 3 cases of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have shown that at the prodromal stage the DLB patients had no pathological profile. 3 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source
The use of Aβ42/Aβ40 ratio rather than Aβ42 alone could contribute toward pre-analytical standardization, thus allowing the general use of CSF AD biomarkers in routine practice. 1 key finding →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that a capsaicin-rich diet may exert favorable effects on AD blood biomarkers and cognitive function in middle-aged and elderly adults. 3 key findings →
Participants: 338 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia around the world (~ 65%). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is the first study to our knowledge demonstrating an association between cognitive function and CSF orexin A levels in AD. 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
Ultrasensitive assays have been developed which enable biomarkers of Alzheimer's disease pathology and neurodegeneration to be measured in blood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hematopoietic stem cells contribute to mammalian brain tissue regeneration by transdifferentiation processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
High-throughput plasma Aβ42/40 LC-MS/MS assays can help identify patients with low likelihood of AD pathology, which can reduce PET evaluations, allowing for cost savings. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest a temporal sequence of events in App NL-F/NL-F knock-in mice, in which initial deposition of Aβ aggregates in the brain is followed by a decline of the Aβ42/Aβ40 ratio in CSF and serum once the cerebral Aβ pathology becomes significant. 4 key findings →
Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
ECM proteins do not reflect AD-pathology in CSF. 2 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of inflammatory processes has been observed within the brain as well as periphery of subjects with Alzheimer's disease (AD). 3 key findings →
Participants: 153 Evidence: low
Full summary, score breakdown and related studies → Original source
These data indicate that the AD genetic architecture influences cognitive and CSF phenotypes in DS adults, supporting common pathways that influence memory decline in both traits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Except for Aβ42/40, plasma biomarkers are heritable. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of the amyloid-β (Aβ) peptides (Aβ42/Aβ40) into amyloid fibrils and plaques is one of the molecular hallmarks in dementia and Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Offspring with a family history of LOAD on the maternal side have lower Aβ42 and Aβ42/40 ratio in the CSF, and maybe at higher risk for developing AD. 3 key findings →
Participants: 162 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β and alpha 1-antichymotrypsin (ACT) play an important role in the pathogenesis of sporadic Alzheimer's disease (AD). 2 key findings →
Participants: 112 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 →