29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
An (18)F-labeled PET amyloid-beta (Abeta) imaging agent could facilitate the clinical evaluation of late-life cognitive impairment by providing an objective measure for Alzheimer disease (AD) pathology. 4 key findings →
Design: open-label trial Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ARIA-positive patients had significantly higher Fazekas scores compared with ARIA-negative patients (1.37 versus 1.0; P = .0262), indicating a greater DWMH burden. 5 key findings →
Design: cohort study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Outdoor activity is linked to lower dementia risk, particularly in those living in more accessible GS. 5 key findings →
Design: longitudinal study Participants: 187,724 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (SVD) is recognized as a major vascular contributor to cognitive decline, ultimately leading to dementia and stroke. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sensitivity analyses were performed to validate the robustness of the linear regression results. 4 key findings →
Design: longitudinal study Participants: 832 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The reliable worsening method produced a cut point only for amyloid PET. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities predict an increased risk of stroke, dementia, and death.
Full summary, score breakdown and related studies → Original source Free full text
Positron emission tomography (PET) of brain amyloid b is a technology that is becoming more available, but its clinical utility in medical practice requires careful definition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Regions with high-average SUVR are not necessarily those with the greatest tau pathology. 1 key finding →
Participants: 490 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
Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lower PiB uptake accurately distinguishes cases with LBD from cases with AD or mixed pathology, correlating with the Thal Aβ phase. 2 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females. 4 key findings →
Design: cross-sectional Participants: 148 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that the presence of objective memory impairment in patients with probable CAA could serve as a marker for underlying tau pathology. 4 key findings →
Design: cross-sectional Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-related frailty and disease-related frailty may represent different degrees of frailty severity on a biological level. 5 key findings →
Design: cross-sectional Participants: 1,199 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →
Design: cross-sectional Participants: 276 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration. 3 key findings →
Participants: 373 Evidence: moderate
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
Within a heterogenous group of MCI patients, including many with clinically significant CVD, baseline memory and executive performance significantly predicted likelihood to develop dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →
Participants: 399 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our objective was to investigate cross-sectional associations between odor identification ability and imaging biomarkers of neurodegeneration and amyloid deposition in clinically normal (CN) elderly individuals, specifically testing the hypothesis that there may be an interaction between amyloid deposition and neurodegeneration in predicting odor identification dysfunction. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Education, occupation, premorbid intelligence, and brain size are surrogate markers for cognitive reserve. 1 key finding →
Design: longitudinal study Participants: 819 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
An eight-week course of IVIG totaling 2 g/kg in MCI is safe but is not sufficient to sustain an initial reduction in brain atrophy or a temporary delay in conversion to dementia at five years. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Two decades of epidemiological research shows that silent cerebrovascular disease is common and is associated with future risk for stroke and dementia. 3 key findings →
Evidence: high
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.
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →