27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that a hearing intervention might reduce cognitive change over 3 years in populations of older adults at increased risk for cognitive decline but not in populations at decreased risk for cognitive decline. 5 key findings →
Design: randomized controlled trial Participants: 858 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
ACHIEVE-P sets the stage for the full-scale ACHIEVE trial (N = 850, recruitment beginning November 2017), the first randomized trial to determine efficacy of a best practices hearing (vs. successful aging) intervention on reducing cognitive decline in older adults with HL. 1 key finding →
Design: randomized controlled trial Participants: 850 Evidence: high
Full summary, score breakdown and related studies → Original source
Midlife vascular risk factors are associated with increased risk of dementia in black and white ARIC Study participants. 4 key findings →
Design: prospective cohort Participants: 744 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This randomized trial gave hearing aids plus counseling, or only general health education, to 977 older adults with untreated hearing loss, then tracked cognition for three years. 4 key findings →
Design: RCT Participants: 977 Evidence: moderate
Full summary, score breakdown and related studies → Original source
When completed in 2022, Aging and Cognitive Health Evaluation in Elders study should provide definitive evidence of the effect of hearing treatment versus education control on cognitive decline in community-dwelling older adults with mild-to-moderate hearing impairment. 3 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
The prediction algorithms are a first but promising step toward providing specific prognoses to patients, families, and practitioners. 1 key finding →
Design: cohort study Participants: 236 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study Participants: 271 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AD-signature cortical thinning in CN-AD converters in both samples was remarkably similar, about 0.2 mm (p 1). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Diabetes status, poor glycemic control, and longer diabetes duration were associated with worse cognitive outcomes over a median follow-up of 5 years. 4 key findings →
Participants: 5,099 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From a longitudinal study of normal (Clinical Dementia Rating [CDR] = 0; n = 77) and mildly impaired (CDR = 0.5; n = 167) participants with 5 or more annual clinical assessments, baseline level of cognitive impairment in daily life was graded using CDR sum of boxes (CDR-SB) and level of cognitive performance impairment was graded using neuropsychological test scores. 4 key findings →
Design: longitudinal study Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
High WMH was a predictor of progression from normal to MCI (adjusted hazard ratio [HR], 3.30; 95% confidence interval [CI], 1.33-8.17; P= .01) but not conversion from MCI to all-cause dementia. 2 key findings →
Design: cohort study Participants: 67 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Of 9,033 ARIC participants with sufficient Medicare coverage data (4,980 [55.1%] female, 1993 [22.1%] Black), 671 met the definition of LOE. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The new criteria for AD are presented in three documents. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These data support distinct processes in the initiation and progression of AD pathology within the temporal cortex: Deposition of Abeta reaches a "ceiling" early in the disease process, whereas NFT formation, synaptic loss, and gliosis continue throughout the course of the illness. 1 key finding →
Evidence: moderate
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An international group of clinical and basic scientists participated in the Frontotemporal Dementia and Pick's Disease Criteria Conference at the National Institutes of Health in Bethesda, Md, on July 7, 2000, to reassess clinical and neuropathological criteria for the diagnosis of frontotemporal dementia (FTD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Markers of lower socioeconomic status predict risk of developing incident AD. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results demonstrate that temporoparietal regions show differential rates of atrophy on MRI during prodromal Alzheimer disease (AD). 5 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CMBs are a common vascular pathology in the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The results suggest that the hippocampus and the temporal horn of the lateral ventricles may be useful as antemortem markers of AD in mildly impaired patients. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent studies indicate that impairments in two cognitive domains characterize the cognitive abnormalities that appear earliest in the course of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical hallmark of Alzheimer's disease (AD) is a gradual decline in cognitive function. 1 key finding →
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →