PS2V levels increased in AD postmortem brain but PS2V was also present at significant levels in FTD and LBD brains. 4 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
PS2V levels increased in AD postmortem brain but PS2V was also present at significant levels in FTD and LBD brains. 4 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (FAD) is characterized by a positive family history of dementia and typically occurs at an early age with an autosomal dominant pattern of inheritance. 2 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
As of 2023, it is estimated that 6.7 million individuals in the United States live with Alzheimer's disease (AD). 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
The dominant theory of Alzheimer disease (AD) has been that amyloid-β (Aβ) accumulation in the brain is the initial cause of the degeneration leading to cognitive and functional deficits. 3 key findings →
Participants: 144 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous genome-wide association studies have identified numerous genetic variants and revealed the genetic architecture of educational attainment, another marker of cognitive reserve. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The adjusted hazard ratio (HR) of dementia for a 5-μg/m3 increase in NO2 was 1.09 (95% CI, 1.05-1.14); the adjusted HR of dementia for a 1-μg/m3 increase in PM2.5 was 1.10 (1.04-1.17). 5 key findings →
Participants: 447 Evidence: low
Full summary, score breakdown and related studies → Original source
To better characterize the potential biological mechanisms underlying insulin resistance (IR) and dementia, we derive cross-population and population specific polygenic scores [PSs] for fasting insulin and IR-related partitioned PSs [pPSs]. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular deposition of the amyloid beta-peptide, leading to intracerebral hemorrhage in severe cases. 4 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cross-sectional positron emission tomography (PET) studies find that cognitively normal carriers of the apolipoprotein E (APOE) epsilon4 allele, a common Alzheimer's susceptibility gene, have abnormally low measurements of the cerebral metabolic rate for glucose (CMRgl) in the same regions as patients with Alzheimer's dementia. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TT genotype of rs688 in the LDLR gene was not found to be associated with elevated levels of total cholesterol or LDL-C. 4 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that stakeholders in AD prevention research generally wish to know biological test information about their risk for developing AD to assist in making life plans. 5 key findings →
Participants: 207 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide association studies (GWAS) of cerebrospinal fluid (CSF) Alzheimer's Disease (AD) biomarker levels have identified novel genes implicated in disease risk, onset and progression. 4 key findings →
Participants: 1,467 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
GWAS found the associations of two single nucleotide polymorphisms (rs7943454 and rs640476) with plasma NFL at suggestive levels. 5 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated threonine 181 of tau (pTau181) and amyloid beta (Aβ) are biomarkers for differential diagnosis and preclinical detection of Alzheimer disease (AD). 2 key findings →
Participants: 2,086 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (apoE) type 4 allele (APOE4) is a susceptibility gene for late-onset familial and sporadic Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (apoE) genotype has a major influence on the risk for Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E4 (APOE4) allele is associated with an early age of onset of the nonfamilial form of Alzheimer disease (AD) and with increased beta protein amyloid deposition in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We examined the association of mtDNA variation with Alzheimer disease (AD) risk in Caucasians (989 cases and 328 controls) testing the effect of individual haplogroups and single nucleotide polymorphisms (SNPs). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We scanned throughout chromosome 21 to assess genetic associations with late-onset Alzheimer disease (AD) using 374 Japanese patients and 375 population-based controls, because trisomy 21 is known to be associated with early deposition of beta-amyloid (Abeta) in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite the success of large-scale genome-wide association studies (GWASs) on complex traits, our understanding of their genetic architecture is far from complete. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Only Apolipoprotein E polymorphisms have been consistently associated with the risk of late-onset Alzheimer disease (LOAD), but they represent only a minority of the underlying genetic effect. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of the amyloid β (Aβ) peptide within the brain is hypothesized to be one of the main causes underlying the pathogenic events that occur in Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia with Lewy bodies (DLB) is pathologically characterized by α-synuclein aggregates in the brain. 1 key finding →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Inheritance of apolipoprotein E4 (APOE4) is a major risk factor for development of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although the mechanism underlying vulnerability of white matter tracts in APOE epsilon4 carriers is still unknown, these findings suggest that increased genetic risk for developing Alzheimer disease is associated with changes in microscopic white matter integrity well before the onset of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →