A mutation at codon 717 of the beta-amyloid precursor protein gene has been found to cosegregate with familial Alzheimer's disease in a single family. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
47/100
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by decreased amyloid-beta (Aβ) clearance, enhanced Aβ aggregation, an increased risk of amyloid-related imaging abnormalities (ARIA), and blood-brain barrier (BBB) dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinergic neuron loss is a cardinal feature of Alzheimer disease. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
We confirm that variation in/near APOE/TOMM40 (P = 6 × 10(-14)) alters PCA risk, but with smaller effect than for typical AD (PCA: odds ratio [OR] = 2.03, typical AD: OR = 2.83, P = .0007). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p < 0.05) and LAD (1006 +/- 727 pg/mL; p < 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p < 0.05), and tended to be increased in FTD compared with EAD. 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous trials have shown promising effects of intranasally administered insulin for adults with Alzheimer's disease dementia (AD) or amnestic mild cognitive impairment (MCI). 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Large studies (e.g. UK Biobank) are increasingly used for GWAS and Mendelian randomization (MR) studies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In a multivariate analysis, associations of MS4A6A (rs610932; odds ratio = 0.632, Bonferroni corrected P = .019) and CD33 (rs3865444; odds ratio = 1.492, Bonferroni corrected P = .017) with LOAD were replicated successfully. 5 key findings →
Participants: 1,224 Evidence: low
Full summary, score breakdown and related studies → Original source
Over the course of an individual’s lifetime, genomic alterations accumulate in somatic cells. 3 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have identified a number of risk variants for Alzheimer’s disease implicated in inflammatory responses (Bettens et al., 2013); exome sequencing has revealed polymorphisms in the microglial receptor TREM2 gene as a rare but significant risk for Alzheimer’s disease (Guerreiro et al., 2013; Jonsson et al., 2013); and recently, the CD33 risk allele has been shown to inhibit microglial clearance of amyloid-β (Bradshaw et al., 2013; Griciuc et al., 2013). 5 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disruption, nightly restlessness, sundowning, and other circadian disturbances are frequently seen in Alzheimer's disease (AD) patients. 2 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Missense mutations in the alpha-synuclein gene cause familial Parkinson's disease (PD), and alpha-synuclein is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease (AD). 3 key findings →
Participants: 65 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) synaptosomal-associated protein 25 (SNAP-25) and neurogranin (Ng) are recently described biomarkers for pre- and postsynaptic integrity known to be elevated in symptomatic Alzheimer disease (AD). 2 key findings →
Participants: 274 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroimaging features of early-onset AD in comparison to late-onset AD include greater frequency of hippocampal sparing and posterior neocortical atrophy, increased tau burden, and greater connectomic changes affecting frontoparietal networks rather than the default mode network. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both apolipoprotein E (apoE) and 24(S)-hydroxycholesterol are involved in the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Advances in human genetics have implicated a growing number of genes in neurodegenerative diseases, providing insight into pathological processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The cholesterol transporter ATP-binding cassette transporter A1 (ABCA1) moves lipids onto apolipoproteins including apolipoprotein E (apoE), which is the major cholesterol carrier in the brain and an established genetic risk factor for late-onset Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies indicate that impairments in two cognitive domains characterize the cognitive abnormalities that appear earliest in the course of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The discovery that the epsilon 4 allele of the apolipoprotein E (apoE) gene is a putative risk factor for Alzheimer disease (AD) in the general population has highlighted the role of genetic influences in this extremely common and disabling illness. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The genetics of Alzheimer disease (AD) to date support an age-dependent dichotomous model whereby earlier age of disease onset ( or = 65 years) representing most cases of AD has yet to be explained by a purely genetic model. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
46/100
Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD)-like neuropathology increases progressively during aging in most primates, and, in some species, is concurrent with reproductive decline in females and cognitive impairments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Linkage studies, candidate gene and whole-genome association studies have resulted in a tremendous amount of putative risk genes for Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
- Association of apolipoprotein E gene with risk, cognition, and prognosis of epilepsy
- Polygenic risk score analysis of pathologically confirmed Alzheimer disease
- Additive Effects of White Matter Hyperintensity and APOE ε4 Status on Risk of Incident Dementia in Two Large Longitudinal Cohorts
- Glucocerebrosidase Activity Modulates Neuronal Susceptibility to Pathological α-Synuclein Insult
- Relationship between ApoE, MRI findings, and cognitive function in the Cardiovascular Health Study
- APOE effect on Alzheimer's disease biomarkers in older adults with significant memory concern
- Candidate Gene for the Chromosome 1 Familial Alzheimer's Disease Locus
- Cognitive activity and incident AD in a population-based sample of older persons
- TDP-43 proteinopathies: a new wave of neurodegenerative diseases
- Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer's disease
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 →