The cause of progressive supranuclear palsy (PSP) is not known and has been little studied. 4 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The cause of progressive supranuclear palsy (PSP) is not known and has been little studied. 4 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
SIs on the LASSI-L related to PSI and frPSI uniquely differentiated Amy+ and Amy- participants with aMCI and likely reflect deficits with inhibition and source memory in preclinical AD not captured by traditional cognitive measures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Navigation testing in real space is a promising approach to identify patients with aMCI with underlying Alzheimer pathology. 2 key findings →
Evidence: low
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Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS. 4 key findings →
Participants: 27 Evidence: low
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Among 428 older autopsied persons (mean age at death = 91 years, 70% women) considered for anti-amyloid treatment eligibility assessment, 58% had MCI and 42% had mild-stage Alzheimer dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy. 5 key findings →
Evidence: low
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Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The navigation disability in Alzheimer disease and mild cognitive impairment (MCI) involves a selective impairment of spatial cognition and is associated with atrophy of the right-lateralized navigation network. 4 key findings →
Evidence: low
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The structural brain network of patients showed reduced local efficiency compared to controls. 2 key findings →
Evidence: low
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Risk of dementia by age 80 was more pronounced for Hispanic and black men compared with white men. 2 key findings →
Evidence: low
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Little information exists on the performance of black versus white patients with Alzheimer's disease on neuropsychological tests for dementia. 2 key findings →
Participants: 830 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The pattern of cerebral degeneration in Alzheimer's disease (AD) patients suggests that basic auditory capacities should be normal in AD, whereas progressively higher levels of auditory function should be increasingly impaired. 4 key findings →
Evidence: low
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One-hundred nineteen individuals with a family history of AD (Presymptomatic Evaluation of Experimental or Novel Treatments of Alzheimer's Disease [PREVENT-AD] cohort, mean age 67 ± 5 years) underwent tau-PET ([ 18 F]FTP), β-amyloid (Aβ)-PET ([ 18 F]NAV4694 [NAV]), and cognitive assessment. 4 key findings →
Evidence: moderate
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Concentrations of phosphorylated tau181, total tau (t-tau), and β-amyloid in the CSF were measured in 3 groups: 22 former professional athletes with multiple concussions (mean ± SD age 55.9 ± 12.2 years), 5 healthy controls (age 57.4 ± 5.2 years), and 12 participants (age 60.0 ± 6.6 years) diagnosed with Alzheimer disease (AD). 4 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) provides ratings of an individual's changes in everyday cognitive functions during the previous 10 years. 4 key findings →
Participants: 399 Evidence: low
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The presence of the APOE epsilon 4 allele encoding apolipoprotein E4 (apoE4) is the major genetic risk factor for late-onset Alzheimer's disease (AD). 4 key findings →
Evidence: low
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We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration. 5 key findings →
Participants: 1,542 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.001), with the automated approach more likely to classify a scan as tau negative and lower agreement between methods in more severe cases and AD clinical variants. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.035), consistent with a neurodegenerative pattern. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.026). Complementing previous research that focuses on CSVD and white matter changes, our study highlights abnormal gray matter integrity as a possible link between small vessel pathology and cognitive disorders. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The authors describe a novel missense mutation in the presenilin 2 (PSEN2) gene at residue 439 that predicts an aspartate-to-alanine substitution (D439A). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors describe a 28-year-old woman with histopathologically confirmed early onset Alzheimer disease characterized by severe frontal lobe involvement associated with a de novo mutation in the presenilin 1 gene (PSEN1). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the last 2 years, there have been 3 successful trials of antiamyloid antibodies in Alzheimer disease (AD): aducanemab, now controversially US Food and Drug Administration-approved under the accelerated approval pathway1; lecanemab, now FDA-approved2; and donanemab, now going through the approval process.3 All 3 share a common broad mechanism, that is, antibody-mediated removal of β-amyloid (Aβ) from the brain, and this is almost certainly the basis of their therapeutic action.4 When used in the earliest symptomatic stages of AD, all have modest clinical effects, all clear Aβ from the brain, and all show evidence for some changes in molecular markers believed to be downstream of Aβ accumulation in keeping with disease modification.4 However, all these drugs-and several other antiamyloid immunotherapies that failed to show positive effects in clinical trials (e.g. bapineuzemab and gantenerumab)5,6-have the troubling adverse event of antibody-related imaging abnormalities (ARIA). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Forty-one participants (30 male, 11 female) with a mean (SD) age at death of 75.7 (10.6) years were included. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The average age at LP was 79.3 years (SD = 5.6), and the average age at death was 87.1 years (SD = 6.5). 2 key findings →
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 27,380 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 →