The trial occurred during the COVID-19 pandemic. 5 key findings →
Design: randomized controlled trial Participants: 106 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study investigated a subtype of reactive astrocytes called A1 and discovered that they are induced by classically activated neuroinflammatory microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by amyloid-beta (Aβ) accumulation and neuroinflammation. 4 key findings →
Design: clinical trial Participants: 21 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Detection of Alzheimer's disease (AD) before the development of clinical symptoms is critical for enabling the use of new treatments. 2 key findings →
Participants: 551 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MES-defined cognitive impairment (≤-2 standard deviation [SD] deviation after adjustment for demographics) was identified in 12.4% of participants. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
P-tau181 (odds ratio [OR] 2.06, 95% confidence interval [CI] 1.41-3.00, p < 0.001), p-tau217 (OR 1.70, 95% CI 1.10-2.61, p = 0.016), and t-tau (OR 1.44, 95% CI 1.08-1.92, p = 0.012) were associated with appetite change. 5 key findings →
Design: cross-sectional Participants: 1,005 Evidence: low
Full summary, score breakdown and related studies → Original source
Presence on T2-weighted images of white matter hyperintensities (WMH) has been previously shown to be more commonly associated with GRN mutations rather than other forms of FTD. 5 key findings →
Design: longitudinal study Participants: 336 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain volume analyses included 622 participants (mean age ± SD: 70.9 ± 10.2) with an average of 3.3 MRI scans over 4.7 years. 5 key findings →
Design: longitudinal study Participants: 622 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dilation of perivascular spaces (PVS) in the brain may indicate poor fluid drainage due to the accumulation of perivascular cell debris, waste, and proteins, including amyloid-beta (Aβ). 2 key findings →
Design: longitudinal study Participants: 56 Evidence: moderate
Full summary, score breakdown and related studies → Original source
68/100
Atypical and typical AD patients were comparable for Aβ42/40 values. 4 key findings →
Design: retrospective cohort Participants: 39 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We included 400 middle-aged CU participants, of whom 135 (33.8%) were CSF Aβ-positive. 5 key findings →
Design: cross-sectional Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In participants who progressed to amyloid-positive MCI, plasma p-tau181/Aβ42 and GFAP diverged from stable controls earliest (about 13 and 12 years before symptom onset, respectively), followed by Aβ42/Aβ40, p-tau181, and NfL, all of which became abnormal before symptom onset. 4 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The AD PRS model that was most predictive of AD diagnosis (even without APOE) was the liver AD PRS: n = 1,115; odds ratio = 2.15 (1.67-2.78), p = 3.62×10-9. 3 key findings →
Design: cohort study Participants: 1,115 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The BHA-CS was accurate at detecting cognitive impairment and exhibited excellent long-term stability. 4 key findings →
Design: longitudinal study Participants: 340 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive impairment is recognised as an important non-motor symptom in Parkinson's disease (PD) and there is a need for evidence-based non-pharmacological interventions that may prevent or slow cognitive decline in this patient group. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
In addition to the apolipoprotein E (APOE) locus, our GWAS of two independent Chinese samples uncovered three novel AD susceptibility loci (KIAA2013, SLC52A3, and TCN2) and a novel ancestry-specific variant within EGFR (rs1815157). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, 19 susceptibility loci for Alzheimer's disease (AD) had been identified through AD genome-wide association studies (GWAS) meta-analysis. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We found that a higher PGS was associated with higher rates of tau-PET accumulation, in particular at elevated amyloid-PET levels. 4 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It is estimated that the impact of related genes on the risk of Alzheimer's disease (AD) is nearly 70%. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The association between PICALM rs3851179 variant and Alzheimer's disease (AD) has been well established by previous genome-wide association studies (GWAS) and candidate gene studies in European population. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The Brains for Dementia Research project is a recently established longitudinal cohort which aims to provide brain tissue for research purposes from neuropathologically defined samples. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Dementia is a leading cause of death in many countries. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
53/310 (17.1%) subjects were classified as Focal-FMM. 5 key findings →
Design: longitudinal study Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study analyzed 871 eyes from 439 participants (230 APOE ε4 noncarriers and 209 carriers). 5 key findings →
Design: longitudinal study Participants: 58 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →