27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Late-onset Alzheimer's disease (AD; LOAD) is the most common human neurodegenerative disease, however, the availability and efficacy of disease-modifying interventions is severely lacking. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of age-related dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Considerable variations of breadth and intensity in county-level HCBS were observed. 4 key findings →
Participants: 365,310 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 1 key finding →
Participants: 2,247 Evidence: low
Full summary, score breakdown and related studies → Original source
A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) with synaptic dysfunction identified as an early pathological hallmark. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
There is a dearth of studies on the genetics of AD in the Arab world. 4 key findings →
Design: systematic review Participants: 2,173 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
BIOFACE is a two-year study of clinical, cognition, and biomarkers that will shed light on the physiopathology and the potential utility of plasma and NPEs as non-invasive early diagnostic and prognostic biomarkers in people younger than 65 years. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings lend support to a model in which fibrillar Aβ is still accumulating in the early stages of clinical disease but approaching a relative plateau, a point at which Aβ may uncouple from neurodegenerative processes including synaptic loss. 5 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Widespread cortical reduction of synaptic density was documented in a cohort of DLB/PDD subjects using in vivo [11C]UCB-J PET. 5 key findings →
Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multidomain intervention studies conducted so far appear to have mixed results and substantial variability in target populations, format and intensity of interventions, choice of control conditions, and outcome measures. 2 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and other dementias are now the seventh leading cause of death in the world and are projected to affect 115.4 million people by 2050. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
The actual role of SARS-CoV-2 in brain damage remains controversial due to lack of matched controls. 2 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive decline is a broad syndrome ranging from non-pathological/age-associated cognitive decline to pathological dementia. 5 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Of 3123 decedents, 465 (14.9%) had a primary hospice diagnosis of dementia and 943 (30.2%) had comorbid dementia and died of another illness. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
In non-demented individuals along the AD continuum, p-tau drives cognitive dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an urgent need to establish blood biomarkers for Alzheimer's disease (AD). 4 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
Detecting early signs of cognitive decline is crucial for early detection and treatment of Alzheimer's Disease. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Although there were no significant changes in caregiver burden, we were encouraged by the increased emotional well-being of our participants following the completion of our program. 4 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
Both DELPHI analysis of network function and DTI analysis detected a significant decrease in connectivity, excitability, and WM integrity in the SCD group compared to healthy control (HC) subjects; a significant decrease was also noted for aMCI and Dementia groups compared to HC. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation. 5 key findings →
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
Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Synaptic disturbances in excitatory to inhibitory (E/I) balance in forebrain circuits are thought to contribute to the progression of Alzheimer's disease (AD) and dementia, although direct evidence for such imbalance in humans is lacking. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Asthma participants had widespread and large-magnitude differences in several dMRI metrics, which were indicative of neuroinflammation and neurodegeneration, and which were robustly associated with GFAP and, to a lesser extent, NfL. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
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 →