Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Pericytes are critical for maintaining blood-brain barrier (BBB) integrity and have emerged as key contributors to Alzheimer's disease (AD) pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Microglia are central mediators of neuroinflammation in Alzheimer's disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling. 5 key findings →
Participants: 204 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher AD-PRS was associated with faster CD in the full clinical cohort and in biomarker subset, independently of APOE genotype. 5 key findings →
Design: longitudinal study Participants: 7,233 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Pivotal trials demonstrated statistically significant but modest average slowing of decline: Clarity AD showed a 0.45-point between-group difference in CDR-SB worsening at 18 months, and TRAILBLAZER-ALZ 2 showed a 3.25-point iADRS difference in the low/medium-tau population at 76 weeks. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Compared with men, women had greater amyloid burden (B = 0.05; 95% CI, 0.02-0.07; P < .001), Braak stages III and IV (B = 0.05; 95% CI, 0.02-0.08; P = .003) and Braak stages V and VI (B = 0.09; 95% CI, 0.06-0.12; P < .001) tau burden, and AD signature thickness (B = 0.04; 95% CI, 0.02-0.05; P < .001). 5 key findings →
Design: cross-sectional Participants: 501 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
45/100
Among 5712 adults (mean [SD] age, 63.47 (8.15) years; unweighted 3663 [53.92%] female), higher ln(ptau-181) was associated with ECog-12 memory (unstandardized β = 0.088; 95% CI, 0.005-0.170). 5 key findings →
Design: cross-sectional Participants: 5,712 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Thirty-two patients met inclusion criteria (lecanemab, N=15; donanemab, N=17). 5 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Individuals with Alzheimer's disease (AD) are at an increased risk of bone fracture, while osteoporosis in women is one of the earliest predictors of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified APOE2 allele as linked to exceptional longevity, with carriers exhibiting a reduced risk of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has a strong genetic predisposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lysosomal dysfunction in myeloid cells is increasingly implicated in neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among most Latinos in northern Manhattan who learned they had an APOE ε4/ε4 genotype, disclosure did not provoke elevated levels of distress. 3 key findings →
Participants: 61 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
43/100
Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight normative modelling's utility in revealing the complex interplay among sex, age, and AD risk in shaping brain structure and cognition in later life. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AD risk was associated with shorter TL (β = -0.48, P < 2 × 10–16). 5 key findings →
Participants: 6,973 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Over 15 years of follow-up (UKB), moderate or high CVH versus low CVH was associated with a lower risk of MCI (hazard ratio 0.82 [95% CI 0.71, 0.95], P < 0.05) but not with risk of all-cause dementia (0.97 [0.84, 1.11], P = 0.63). 4 key findings →
Participants: 41,374 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →
Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Late-life dementia has a strong heritable component. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Identity-by-descent (IBD) mapping provides complementary signals to genome-wide association studies (GWASs) when multiple causal haplotypes or variants are present but not directly tested. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early and accurate prognosis of Alzheimer’s disease (AD) remains limited by current biomarkers, which are often invasive, require expensive equipment, or fail to predict individual trajectories of cognitive decline. 2 key findings →
Participants: 459 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Using a 2-sample Mendelian randomization (MR) approach, we evaluated MR evidence for genetically proxied effects of 10 pre-specified gut bacterial classes on type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD), and assessed MR evidence for a direct genetically proxied effect of T2DM on AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →