Immunotherapeutics targeting amyloid-β (Aβ) have had mixed results in clinical trials. 3 key findings →
Participants: 5,554 Evidence: high
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Immunotherapeutics targeting amyloid-β (Aβ) have had mixed results in clinical trials. 3 key findings →
Participants: 5,554 Evidence: high
Full summary, score breakdown and related studies → Original source
The efficacy and safety of anti-amyloid mAbs in AD may differ based on patients' demographic and genetic factors. 4 key findings →
Design: systematic review Participants: 5,633 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 210 participants were enrolled and 82% completed 26 weeks of treatment. 5 key findings →
Design: clinical trial Participants: 210 Evidence: high
Full summary, score breakdown and related studies → Original source
No significant difference in ADAS-Cog13, CDR Sum of Boxes (CDR-SOB), or FAQ scores were found between treatment groups at 3 and 6 months. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Between Dec 8, 2009, and Dec 23, 2011, we randomly allocated 278 patients to treatment: 133 to placebo and 145 to idalopirdine. 132 patients in the placebo group and 140 in the experimental group were included in the final analysis. 5 key findings →
Design: clinical trial Participants: 278 Evidence: high
Full summary, score breakdown and related studies → Original source
Among 14 placebo-controlled trials of elderly patients with dementia reporting a total global outcome score that includes symptoms such as psychosis, mood alterations, and aggression, small but statistically significant effects sizes ranging from 0.12 and 0.20 were observed for aripiprazole, olanzapine, and risperidone. 5 key findings →
Design: systematic review Participants: 1,000 Evidence: high
Full summary, score breakdown and related studies → Original source
The risk-benefit profile of anti-Aβ monoclonal antibodies (mAbs) in Alzheimer's disease (AD) remains unclear, especially concerning their safety and overall effects on AD progression and cognitive function. 4 key findings →
Design: meta-analysis Participants: 14,980 Evidence: high
Full summary, score breakdown and related studies → Original source
In participants with prodromal to mild AD in this randomized clinical trial, semorinemab did not slow clinical AD progression compared with placebo throughout the 73-week study period but did demonstrate an acceptable and well-tolerated safety profile. 3 key findings →
Design: clinical trial Participants: 422 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
ARIA was detected more often on MRI scans when every scan was reviewed by trained neuroradiologists and results adjudicated. 4 key findings →
Participants: 242 Evidence: high
Full summary, score breakdown and related studies → Original source
Three donepezil, two galantamine, one rivastigmine, and two memantine trials, comprising 3093 patients on the study drugs and 2090 patients on placebo, met the selection criteria. 2 key findings →
Design: systematic review Participants: 3,093 Evidence: high
Full summary, score breakdown and related studies → Original source
We aimed to assess whether continued treatment with antipsychotics in people with AD is associated with an increased risk of mortality. 5 key findings →
Participants: 165 Evidence: high
Full summary, score breakdown and related studies → Original source
Group 3 showed less decrease in the SIB score at 12 and 24 weeks compared with group 1 (P < 0.05). 5 key findings →
Design: clinical trial Participants: 31 Evidence: high
Full summary, score breakdown and related studies → Original source
No clinically important adverse events were associated with treatment. 2 key findings →
Design: clinical trial Participants: 432 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These results show that in addition to APOE ε4 allele count, severity of Aβ neuropathology and comorbid cerebrovascular pathology may be relevant for clinicians prescribing anti-Aβ monoclonal antibodies for early AD and developing individualized safety monitoring plans. 2 key findings →
Design: clinical trial Participants: 985 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The most common anticholinergic classes used were tricyclic antidepressants, first-generation antihistamines, and bladder antimuscarinics. 4 key findings →
Design: cohort study Participants: 3,434 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
No significant difference was seen in cognitive and functional decline between early and delayed treatment groups. 4 key findings →
Design: clinical trial Participants: 85 Evidence: high
Full summary, score breakdown and related studies → Original source
SC gantenerumab at doses of up to 1,200 mg Q4W were well tolerated in participants with mild AD dementia. 2 key findings →
Design: open-label trial Participants: 225 Evidence: low
Full summary, score breakdown and related studies → Original source
A growing number of investigations are exploring the utility of intranasal insulin as a means of mitigating cognitive decline. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Antipsychotic use compared with non-use in adults with dementia was associated with increased risks of stroke, venous thromboembolism, myocardial infarction, heart failure, fracture, pneumonia, and acute kidney injury, but not ventricular arrhythmia. 5 key findings →
Design: cohort Participants: 173,910 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Gradual up-titration of dose significantly reduced ARIA-E risk while demonstrating comparable pharmacokinetics/pharmacodynamics compared to standard dosing. 5 key findings →
Design: phase-3-trial Participants: 843 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The experimental paradigm was feasible and acceptable. 3 key findings →
Design: randomized controlled trial Participants: 95 Evidence: high
Full summary, score breakdown and related studies → Original source
Antibody administration was well tolerated with doses up to 400 mg weekly. 2 key findings →
Design: clinical trial Participants: 52 Evidence: high
Full summary, score breakdown and related studies → Original source
Our analysis found that lecanemab showed significant positive statistical efficacy with respect to cognition, function, and behavior in patients with early AD though the actual clinical significance is yet to be established. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
According to studies, lecanemab lessens clinical deterioration and reduces brain amyloid-beta plaques (difference,.45; 95% confidence interval,.67 to.23; p < .001). 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The safety profile was similar for 20 μg treatment and placebo patients. 5 key findings →
Design: post-hoc analysis Evidence: high
Full summary, score breakdown and related studies → Original source
10 of the 468 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.
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
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.
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.
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 →