Treatment with donanemab resulted in rapid reduction of amyloid, even after a single dose. 5 key findings →
Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Seventy-one studies were included for review, representing a total of 6757 patients (2350 AD, 793 MCI, 2902 healthy controls (HC), and 841 others with a range of other neurodegenerative diagnoses). 5 key findings →
Design: systematic review Participants: 6,757 Evidence: high
Full summary, score breakdown and related studies → Original source
By aggregating results across samples, this study advances knowledge on the association between personality and neuropathology. 5 key findings →
Design: meta-analysis Participants: 3,015 Evidence: high
Full summary, score breakdown and related studies → Original source
These results suggest that flortaucipir PET scans, when interpreted with an US Food and Drug Administration-approved, clinically applicable visual interpretation method, may provide valuable information regarding the risk of clinical deterioration over 18 months among patients with AD and MCI. 3 key findings →
Design: longitudinal study Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Noninvasive biomarkers of early neuronal injury may help identify cognitively normal individuals at risk of developing Alzheimer's disease (AD). 2 key findings →
Design: longitudinal study Participants: 196 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These outcomes illustrate the potential benefits of rasagiline on clinical and neuroimaging measures in patients with mild to moderate AD. 4 key findings →
Design: longitudinal study Participants: 50 Evidence: high
Full summary, score breakdown and related studies → Original source
74/100
Alzheimer's disease (AD) is a remarkable challenge for healthcare in the 21st century. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Fourteen studies assessing OCT-A in preclinical Alzheimer's disease (AD), mild cognitive impairment, or AD were included. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. 2 key findings →
Design: longitudinal study Participants: 1,612 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that the cognitively unimpaired amyloid-β-negative individuals had significant longitudinal tau accumulation confined to the PET Braak-like stage I (3.9%) and II (2.8%) areas. 4 key findings →
Design: longitudinal study Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Substantial flortaucipir accumulation in temporal regions is greatest in persons aged 65 to 85 years who were CU and had high initial Aβ PET levels, compared with those with lower Aβ levels. 4 key findings →
Design: cohort study Participants: 167 Evidence: moderate
Full summary, score breakdown and related studies → Original source
71/100
The apolipoprotein E gene ( APOE ) is the most important genetic risk factor for sporadic Alzheimer disease, with the ε4 allele being associated with increased cerebral amyloid-β and tau pathologies. 5 key findings →
Design: cohort study Participants: 277 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the leading cause of dementia, and mild cognitive impairment (MCI) is considered the transitional state to AD dementia (ADD) and other types of dementia, whose symptoms are accompanied by altered eye movement. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Higher CSF NfL was associated with decreasing microstructural integrity and WMH. 5 key findings →
Design: longitudinal study Participants: 536 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. 5 key findings →
Design: cohort study Participants: 141 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BIN1-associated AD risk is potentially driven by accelerated tau accumulation in the face of Aβ. 4 key findings →
Design: longitudinal study Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Since tau PET tracers were introduced, investigators have quantified them using a wide variety of automated methods. 1 key finding →
Design: cohort study Participants: 415 Evidence: moderate
Full summary, score breakdown and related studies → Original source
67/100
In preclinical Alzheimer disease, entorhinal hypometabolism is a strong and independent predictor of subsequent cognitive decline, making FDG a potentially useful biomarker to increase power in clinical trials. 5 key findings →
Design: cohort study Participants: 131 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events