We have identified 10 plasma proteins strongly associated with disease severity and disease progression. 3 key findings →
Participants: 1,148 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We have identified 10 plasma proteins strongly associated with disease severity and disease progression. 3 key findings →
Participants: 1,148 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AD biomarkers are useful to predict AD-type dementia in subjects with aMCI and naMCI. 4 key findings →
Participants: 231 Evidence: moderate
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Diabetes and pre-diabetes substantially accelerate the progression from MCI to dementia, and anticipate dementia occurrence by more than 3 years in people with MCI. 3 key findings →
Participants: 302 Evidence: moderate
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The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). 2 key findings →
Participants: 201 Evidence: low
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The mean follow-up period for the cohort was 34 months. 3 key findings →
Evidence: moderate
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When patients with MCI underwent clinical follow-up, 29 progressed to dementia, while 44 remained stable. 2 key findings →
Participants: 73 Evidence: low
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Baseline data of 423 PD patients and 196 HCs yielded no between-group differences in demographic characteristics. 3 key findings →
Evidence: moderate
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[(11)C]PIB retention in the neocortical and subcortical brain regions was significantly higher in AD patients than in age-matched controls. 3 key findings →
Participants: 97 Evidence: low
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors. 1 key finding →
Participants: 519 Evidence: moderate
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Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development. 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is considered as a transition phase between normal aging and Alzheimer's disease (AD). 3 key findings →
Participants: 46 Evidence: low
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These findings confirm that MCI is associated with widespread cortical atrophy. 5 key findings →
Evidence: moderate
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Of 4930 participants, 2052 (41%) had MCI. 5 key findings →
Design: cross-sectional Participants: 4,930 Evidence: moderate
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Blood biomarkers of Alzheimer's disease (AD) are promising for dementia prediction, but their association with progression across intermediate stages of cognitive decline in the general population remains unclear. 3 key findings →
Evidence: moderate
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After disclosure, 27 patients with amyloid-positive SCD+ (median [IQR] age, 70 [66-74] years; gender: 14 men [52%]; median [IQR] education: 15 [13 to 17] years, median [IQR] Mini-Mental State Examination [MMSE] score, 29 [28 to 30]) had higher median (IQR) IES-R total score (10 [2 to 14] vs 0 [0 to 2]; P Conclusions and relevance The disclosure of a positive amyloid-PET result to patients with SCD+ was associated with a bigger psychological change, yet such change did not reach the threshold for clinical concern. 5 key findings →
Participants: 27 Evidence: low
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We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia. 1 key finding →
Participants: 15 Evidence: low
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This article presents recommendations, based on the Grading of Recommendations, Assessment, Development, and Evaluation method, for the clinical application of cerebrospinal fluid (CSF) amyloid-β 1-42 , tau, and phosphorylated tau in the diagnostic evaluation of patients with mild cognitive impairment (MCI). 2 key findings →
Evidence: low
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Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks. 4 key findings →
Evidence: low
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Late-life depression (LLD) is associated with development of different types of dementia. 4 key findings →
Participants: 185 Evidence: low
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Researchers evaluated twenty-one patients diagnosed with MCI using PET studies with (11)C-PIB and (18)F-fluoro-deoxy-glucose (FDG), cognitive assessments, and CSF sampling. 3 key findings →
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Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period. 1 key finding →
Evidence: low
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The brain is the most cholesterol-rich organ in the human body. 5 key findings →
Participants: 32 Evidence: low
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Alzheimer's disease (AD) is the most prevalent form of dementia with an estimated worldwide prevalence of over 30 million people, and its incidence is expected to increase dramatically with an increasing elderly population. 1 key finding →
Participants: 85 Evidence: low
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CSF T-tau and P-tau as well as the APOE epsilon4/epsilon4 genotype are robust predictors of AD and are also associated with a more rapid progression from MCI to AD. 4 key findings →
Participants: 58 Evidence: low
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Two-thirds of MCI-multidomains, but only half of MCI-amnestic progress to AD. 1 key finding →
Evidence: low
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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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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 →
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