No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Growing evidence has suggested an association between sleep duration and Alzheimer's disease (AD), but it is unclear if sleep duration is a manifestation of the AD disease process. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The AddNeuroMed and ADNI cohorts were combined giving a total of 329 healthy controls, 421 mild cognitive impairment patients, and 286 Alzheimer's disease (AD) patients. 4 key findings →
Participants: 329 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mutations in the TAR DNA Binding Protein gene (TARDBP), encoding the protein TDP-43, were identified in amyotrophic lateral sclerosis (ALS) patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The presence of the APOE epsilon 4 allele encoding apolipoprotein E4 (apoE4) is the major genetic risk factor for late-onset Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlap in clinical presentation, neuropathology, and genetic underpinnings. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration. 5 key findings →
Participants: 1,542 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
T2DM is one of the strong risk factors of ADRD but genetic T2DM effect does not contribute to ADRD risk. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Over a median follow-up period of 10.44 years, 725 participants developed incident dementia. 5 key findings →
Participants: 104,572 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolomics has been associated with cognitive decline and dementia, but the relationship between metabolites and brain aging remains unclear. 4 key findings →
Participants: 17,770 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia. 5 key findings →
Participants: 1,072 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) primarily affects older adults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
Eighty (22%) participants were APOE ε4 carriers and 290 (73%) were non-carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified sex differences for several classes of metabolites, such as glycerophospholipids, sphingolipids, and amino acids. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer's disease (AD) risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF levels of apoE2, apoE3, and apoE4 were significantly higher (all nominal P < 10 × 10-5 , false discovery rate < 0.001) and those of tumor necrosis factor-α (TNF-α) were significantly lower (nominal P = 1.39 × 10-6 , false discovery rate < 0.001) in APOE-ε4 carriers than in noncarriers. 3 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic Alzheimer's disease (sAD) is marked by dysregulated lipid metabolism, prominently involving apolipoprotein E (ApoE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical outcomes of severe acute respiratory syndrome 2 (SARS-CoV-2) infection are highly heterogeneous, ranging from asymptomatic infection to lethal coronavirus disease 2019 (COVID-19). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
In humans, apolipoprotein E (apoE) is a polymorphic protein of which three common isoforms can be distinguished, designated apoE2, apoE3, and apoE4. 3 key findings →
Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4-KI mice showed impaired retinal structure, vasculature, function, vision, increased gliosis and neuroinflammation, and downregulation of synaptogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our analysis of common SNVs and indels confirmed known genetic loci at MAPT, MOBP, STX6, SLCO1A2, DUSP10, and SP1, and further uncovered novel signals in APOE, FCHO1/MAP1S, KIF13A, TRIM24, TNXB, and ELOVL1. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
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.
- Type 2 diabetes, APOE gene, and the risk for dementia and related pathologies: The Honolulu-Asia Aging Study
- Linkage of a prion protein missense variant to Gerstmann-Sträussler syndrome
- A randomized controlled trial of disclosing genetic risk information for Alzheimer disease via telephone
- Epigenetic mechanisms in neurological diseases: genes, syndromes, and therapies
- Remote assessments of sleep and cognition in cognitively normal older adults at risk for Alzheimer disease
- Developing a Gene Therapy for the Treatment of Autosomal Dominant Alzheimer's Disease
- Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity
- Genome-wide meta-analysis, fine-mapping and integrative prioritization implicate new Alzheimer's disease risk genes
- Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease
- Familial Alzheimer Dementia: a prevalent disorder with specific clinical features
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →