27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This pipeline analysis shows that target biological processes are more diversified, biomarkers are more regularly used, and repurposed agents are being explored to determine their utility for the treatment of AD. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
All six CTE stage III cases had Braak NFT stage III but no neuritic plaques. 5 key findings →
Design: clinical trial Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
In patients treated up to 36 months, amyloid plaque levels continued to decrease in a dose- and time-dependent manner, with levels in the 10 mg/kg fixed-dose group reaching and remaining below a quantitative cut-point discriminating a positive/negative scan. 1 Reduced amyloid plaque levels were also observed in patients switched from placebo to aducanumab during the LTE. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Overall, 392 patients were enrolled in HARMONY; 49 patients with PDD and 27 patients with DLB were included in the open-label safety analysis, of whom 46 met response criteria and were randomized to receive pimavanserin (n = 22) or placebo (n = 24) during the double-blind period. 4 key findings →
Design: phase-3-trial Participants: 76 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Our trial showed that olfactory-stimulated oxygenation differences in the orbitofrontal cortex detected by fNIRS were associated with cognitive impairment and cognitive-related objectives. 5 key findings →
Design: open-label trial Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that destroys patient memory and cognition, communication ability with the social environment and the ability to carry out daily activities. 4 key findings →
Design: open-label trial Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 43 individuals enrolled, 14 were women (33%); age (mean ± SD) was 73 ± 8.5 years. 5 key findings →
Design: clinical trial Participants: 43 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
PET amyloid levels were consistent with sparse-to-no neuritic amyloid-β plaques in 51% of patients after 2 years of therapy. 3 key findings →
Design: clinical trial Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
N/A. ENGAGE and EMERGE are Phase 3 clinical trials designed to confirm the clinical efficacy and safety profile of aducanumab in individuals with Early AD. 1 key finding →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
In relation to placebo, the last observation in phase 1 showed greater improvement with olanzapine or risperidone on the Neuropsychiatric Inventory total score, risperidone on the Clinical Global Impression of Changes, olanzapine and risperidone on the Brief Psychiatric Rating Scale (BPRS) hostile suspiciousness factor, and risperidone on the BPRS psychosis factor. 5 key findings →
Design: clinical trial Participants: 421 Evidence: low
Full summary, score breakdown and related studies → Original source
For prediction of dementia in MCI, the AD signature cortical thickness biomarker performed better than hippocampal volume. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nearly a dozen monoclonal antibodies (mAbs) directed against beta-amyloid (Aβ) have been developed for the treatment of Alzheimer disease (AD), and most of these mAbs are undergoing clinical trials. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cholesteryl ester transfer protein inhibition (CETP) has been shown to increase levels of high-density lipoprotein cholesterol (HDL-C) and reduce levels of low-density lipoprotein cholesterol (LDL-C). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The median PPA and NPA were 83.4% and 88.9%, respectively, with lower bounds of 2-sided 95% CIs being 50% or greater for all readers. 4 key findings →
Design: clinical trial Participants: 140 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BPs of [(11)C](R)PK11195 and [(11)C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nonclinical data indicate that ACU193 can reduce the toxic effects of amyloid β oligomers. 3 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Lecanemab can be administered without titration with modest incidence of ARIA. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Primary biomarker efficacy endpoints were not statistically significant in either dose group. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Tau neurofibrillary tangles are found in the brains of patients suffering from Alzheimer's disease and other tauopathies. 2 key findings →
Design: clinical trial Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Despite an ever-growing prevalence and increasing economic burden of Alzheimer's disease (AD) and Parkinson's disease (PD), recent advances in drug development have only resulted in minimally effective treatment. 1 key finding →
Design: clinical trial 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
Initial studies suggested that IVIg contained antibodies against monomeric forms of Aβ 5. 5 key findings →
Design: open-label trial Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
From a clinical perspective, these data further support the rationale for physicians to provide effective management of CVD risk factors and for patients to be compliant with such recommendations to possibly prevent cognitive decline/dementia. 4 key findings →
Design: open-label trial Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Object The authors describe the first clinical trial with encapsulated cell biodelivery (ECB) implants that deliver nerve growth factor (NGF) to the cholinergic basal forebrain with the intention of halting the degeneration of cholinergic neurons and the associated cognitive decline in patients with Alzheimer disease (AD). 1 key finding →
Design: open-label trial Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
S. lavandulaefolia Vahl. (Spanish sage) extracts and constituents have demonstrated anticholinesterase, antioxidant, anti-inflammatory, oestrogenic and CNS depressant (sedative) effects all of which are currently relevant to the treatment of Alzheimer's disease (AD). 4 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →