27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genetic investigations and associations with plasma biomarkers of dementia with Lewy bodies (DLB) in East Asian populations are lacking. 4 key findings →
Participants: 151 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Significant interactions were found between APOE ε4 status and mindfulness and social engagement on cognitive reserve, indicating stronger associations for APOE ε4 carriers. 5 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
APOE-ε4 carrier status appears to modify the cross-sectional association between cardiac output and neuropsychological performance such that lower cardiac output relates to poorer performances among carriers of the ε4 allele. 3 key findings →
Design: cross-sectional Participants: 306 Evidence: low
Full summary, score breakdown and related studies → Original source
Among all participants (mean age 66.7 ± 6.5 years, 100% non-Hispanic White), 451 (6.6%) were using statins at baseline. 5 key findings →
Participants: 564 Evidence: low
Full summary, score breakdown and related studies → Original source
The PRS using 131 SNPs had an effect independent of APOE. 5 key findings →
Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD). 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy rate has been correlated with cognitive decline and its genetic modifiers are still unclear. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified 11 loci-5 in H2-non-carriers and 6 in H2-carriers-although none of the MAPT haplotype-specific associations achieved genome-wide significance. 5 key findings →
Participants: 18,841 Evidence: low
Full summary, score breakdown and related studies → Original source
Extensive simulations demonstrated that the proposed approach not only provided accurate selection of single nucleotide polymorphisms (SNPs) with comparable or higher power but also robust control of false positives. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Variations in the human genome have been found to be an essential factor that affects susceptibility to Alzheimer's disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We propose a novel method to identify disease-related genetic variants enriched by imaging endophenotypes, which are the imaging traits associated with both genetic factors and disease status. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Two novel SNPs (rs465401 and rs460420), both near the ADAMTS1 gene on chromosome 21, showed genome-wide significant associations with CSF NFL. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mild-cognitive impairment (MCI) occurs in up to one-fifth of individuals over the age of 65, with approximately a third of MCI individuals converting to dementia in later life. 2 key findings →
Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent genetic progress allows the molecular diagnosis of young-onset dementia, including Alzheimer's disease (AD) and frontotemporal dementia (FTD). 2 key findings →
Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite subjects with Dominantly-Inherited Alzheimer's Disease (DIAD) represent less than 1% of all Alzheimer's Disease (AD) cases, the Dominantly Inherited Alzheimer Network (DIAN) initiative constitutes a strong impact in the understanding of AD disease course with special emphasis on the presyptomatic disease phase. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most frequent diagnosis of neurodegenerative dementia with early (≤65 years) and late (>65 years) onset ages in familial and sporadic patients. 2 key findings →
Participants: 1,148 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared to participants with no APOE-E4 alleles, participants with 1 allele had better thresholds at 4.0 kHz (β = -2.72 dB, P = .013) and 8.0 kHz (β = -3.05 kHz, P = .006), and participants with 2 alleles had better hearing thresholds at 1.0 kHz (β = -8.56 dB, P = .021). 2 key findings →
Design: cross-sectional Participants: 1,833 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic risk modeling for dementia offers significant benefits, but studies based on real-world data, particularly for underrepresented populations, are limited. 3 key findings →
Participants: 610 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tauopathies are age-associated neurodegenerative diseases whose mechanistic underpinnings remain elusive, partially due to a lack of appropriate human models. 1 key finding →
Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarker results confirm cerebrospinal fluid studies reporting increased levels of pancreatic polypeptide and N-terminal protein B-type brain natriuretic peptide in patients with AD and mild cognitive impairment. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (apoE), a plasma apolipoprotein that plays a central role in lipoprotein metabolism, is localized in the senile plaques, congophilic angiopathy, and neurofibrillary tangles of Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease is more than a pure proteopathy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several heterozygous missense mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) have recently been linked to risk for a number of neurological disorders including Alzheimer disease (AD), Parkinson disease, and frontotemporal dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →