28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 are cellular hallmarks of amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Infant ε4 carriers had lower MWF and GMV measurements than noncarriers in precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions, areas preferentially affected by AD, and greater MWF and GMV measurements in extensive frontal regions and measurements were also significant in the subset of 2- to 6-month-old infants (MWF differences, P Conclusions and relevance While our findings should be considered preliminary, this study demonstrates some of the earliest brain changes associated with the genetic predisposition to AD. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The discovery and reliable detection of markers for neurodegenerative diseases have been complicated by the inaccessibility of the diseased tissue--such as the inability to biopsy or test tissue from the central nervous system directly. 2 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous publications indicate that Alzheimer's Disease (AD) related cortical atrophy may develop in asymmetric patterns, with accentuation of the left hemisphere. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There was a significantly higher risk of developing a dementia diagnosis in Hispanic/Latino and NHB participants than NHW participants and comparably increased dementia hazard ratios in the Hispanic/Latino, NHB, and NHW APOE4 carriers than non-carriers (hazard ratio [HR] [95% confidence interval {CI}] 1.54 [1.25-1.91], 1.25 [1.00-1.57], and 1.55 [1.40-1.72]). 5 key findings →
Design: longitudinal study Participants: 9,784 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Fibrillar amyloid-beta (Abeta) is found in the brains of many cognitively normal older people.
Full summary, score breakdown and related studies → Original source Free full text
Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This article introduces a hypometabolic convergence index (HCI) for the assessment of Alzheimer's disease (AD); compares it to other biological, cognitive and clinical measures; and demonstrates its promise to predict clinical decline in mild cognitive impairment (MCI) patients using data from the AD Neuroimaging Initiative (ADNI). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline. 2 key findings →
Participants: 251 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impact (RHI) exposure. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fifty-four participants (~8% response rate) from the MindCrowd web-based cohort (mean age of 62.39 years; 39 females; and 23 APOE ε4 carriers) completed 75 trials of Super G. Results show that Super G performance was significantly associated with each of the targeted risk factors. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The term Precision Aging describes an approach that focuses on multi-domain profiles of risks impacting individual trajectories of age-related cognitive functioning. 3 key findings →
Participants: 555 Evidence: moderate
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →