27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Development of disease-modifying treatments for Alzheimer's disease (AD) has been challenging, with no drugs approved to date. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In the A4 study, solanezumab did not reduce the decline in cognition or function and had no effect on brain amyloid burden. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The diagnosis of Alzheimer's disease can be improved by the use of biological measures. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The results from the gantenerumab phase 3 programs are expected by the end of 2022 and will add critical information to the collective knowledge on the search for effective AD treatments. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
RECENT FINDINGS: In a large autopsy series from a national consortium, multiple neuropathologies of dementia subtypes were common and increased severity of specific NPS during life was associated with greater severity of neuropathology across diagnoses. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The results of the aducanumab studies have not been published in peer-reviewed form and both the analysis presented by Dr Knopman and collaborators and this perspective are based on data presented in 2019 at the Clinical Trials in AD (CTAD) meeting3; both discussions must be seen as tentative until full data are available. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) research has entered a new era with the recent positive phase 3 clinical trials of the anti-Aβ antibodies lecanemab and donanemab. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The symptomatic drugs currently on the market for Alzheimer's disease (AD) have no effect on disease progression, and this creates a large unmet medical need. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
An international task force of investigators from academia, industry, nonprofit foundations, and regulatory agencies met in Monte Carlo, Monaco, on October 31, 2012, to review lessons learned from the recent bapineuzumab and solanezumab trials, and to incorporate insights gained from these trials into future clinical studies. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Based on the data to date, it is difficult to accurately assess the role of aducanumab in patients with MCI or mild AD. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Tau has become an attractive alternative target for passive immunotherapy efforts for Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we found that SIRT1 is closely related to expression of GLP-1R in hippocampus of 3xTg mice. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
High-dose vitamin supplementation reduces homocysteine levels in patients with AD. 2 key findings →
Design: open-label trial Participants: 69 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease (AD) is characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau, which together lead to neurodegeneration and cognitive decline. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The burden of Alzheimer disease (AD) on the US healthcare system is substantial and increasing. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
and neurogranin changes correlated with sabirnetug-AβO target engagement (p ≤ 0.01). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Efforts to develop effective disease-modifying treatments for Alzheimer's disease (AD) have mostly targeted the amyloid β (Aβ) protein; however, there has recently been increased interest in other targets including phosphorylated tau and other forms of tau. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive supranuclear palsy (PSP) is a common cause of atypical parkinsonism and a rapidly progressive disease that greatly burdens both patients and caregivers. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In 2011, a hexanucleotide repeat expansion in the first intron of the C9orf72 gene was identified as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
LMTM given alone increased hippocampal Acetylcholine (ACh) levels, glutamate release from synaptosomal preparations, synaptophysin levels in multiple brain regions and mitochondrial complex IV activity, reduced tau pathology, partially restored ChAT immunoreactivity in the basal forebrain and reversed deficits in spatial learning. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Phases 1 and 2 results facilitated targeted changes in BESI, thus improving its overall usability for the final phase of the study, when real-time notifications and interventions will be implemented. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
AimTo explore the experiences and challenges for residential care home staff when managing the healthcare needs of their residents, in particular those living with dementia. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with early symptomatic Alzheimer's disease showed less cognitive and functional decline with donanemab compared with placebo in a Phase 2 study offering up to 72 weeks of treatment. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In phase 1, the mean system usability scores increased from 65.4 (SD 11.8) in round 1 to 73.8 (SD 15.9) in round 3, exceeding the benchmark of 68. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →