27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Targeting of tau pathology has long been proposed as a potential therapeutic strategy for Alzheimer's disease (AD). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
The PubMed and Embase databases were searched for clinical trials of anti-Aβ immunotherapy published on or before January 12, 2022. 4 key findings →
Design: clinical trial Participants: 9,429 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Plasma phosphorylated Tau 181 (pTau181) and CSF chitinase-3-like protein 1 (YKL-40) increased following semorinemab treatment in both studies. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Methylthioninium (MT) is a tau aggregation inhibitor with therapeutic potential in Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA) were the most common adverse events reported in the phase 3 ENGAGE and EMERGE trials of aducanumab, an anti-amyloid monoclonal antibody. 4 key findings →
Design: clinical trial Participants: 1,691 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The AD drug development pipeline has agents representing a substantial array of treatment mechanisms and targets. 1 key finding →
Design: clinical trial Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to the 2023 pipeline, there are fewer trials (164 vs. 187), fewer drugs (127 vs. 141), fewer new chemical entities (88 vs. 101), and a similar number of repurposed agents (39 vs. 40). 3 key findings →
Design: clinical trial Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Serum concentrations of semorinemab were consistent across studies and showed a dose-proportional increase across the evaluated dose range. 5 key findings →
Design: clinical trial Participants: 8,430 Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
Repurposed drugs provide a rich source of potential therapies for Alzheimer's disease (AD) and other neurodegenerative disorders (NDD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The intersection of metabolic disease and neurodegeneration represents one of the most consequential frontiers in translational neuroscience. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is a chronic neurodegenerative disorder with complex pathophysiology that affects over 50 million people worldwide. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Ranolazine and metformin may be frequently co‐administered in subjects with chronic angina and co‐morbid type 2 diabetes mellitus (T2DM). 2 key findings →
Design: clinical trial Participants: 28 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
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
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
Growing evidence suggests that agonists of the glucagon-like peptide 1 (GLP-1) receptor provide neuroprotection across a range of experimental models of Parkinson's disease (PD) and, recently, a small proof-of-concept, open-label human trial of exenatide in the treatment moderate severity PD appeared to show persistent improvements in motor and cognitive function. 1 key finding →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease that imposes economic and societal burden. 4 key findings →
Design: clinical 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 →