30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Patients with MCI with APOEε4, abnormal CSF τ level, hippocampal and medial temporal lobe atrophy, entorhinal atrophy, depression, diabetes, hypertension, older age, female gender, lower MMSE score and higher ADAS-cog score, had a high risk for the progression to AD. 1 key finding →
Design: meta-analysis Participants: 14,821 Evidence: high
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The association of depression with prevalent MCI and with progression from MCI to dementia, but not with incident MCI, suggests that depression accompanies cognitive impairment but does not precede it. 4 key findings →
Design: cohort study Participants: 2,160 Evidence: moderate
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Among 112 study participants with MCI, mean (SD) age was 76.6 (6.9) years, 55 were women (49.1%), and 27 progressed to dementia (24.1%), with an incidence rate of 121 per 1000 person-years. 3 key findings →
Design: cohort study Participants: 112 Evidence: moderate
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Neuropsychiatric symptoms in MCI are associated with significantly an increased risk of incident dementia and AD. 5 key findings →
Design: cohort study Participants: 1,821 Evidence: moderate
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Previous conclusions of a lack of efficacy for cognitive training in MCI may have been influenced by not clearly defining the intervention. 1 key finding →
Design: systematic review Participants: 305 Evidence: high
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A diagnosis of COPD is associated with an increased risk for MCI, particularly NA-MCI. 5 key findings →
Design: cross-sectional Participants: 1,425 Evidence: moderate
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The MetS was associated with an increased incidence of MCI and progression to dementia. 4 key findings →
Design: longitudinal study Participants: 984 Evidence: moderate
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These findings add to the growing literature to suggest that the degree of functional impairment at baseline is an important predictor of conversion to dementia and may help explain differences in findings between epidemiological and clinic-based studies. 4 key findings →
Design: longitudinal study Participants: 28 Evidence: moderate
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Low daytime SBP was independently associated with a greater progression of cognitive decline in older patients with dementia and MCI among those treated with AHDs. 5 key findings →
Design: cohort study Participants: 172 Evidence: moderate
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This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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There is substantial neuropsychological decline in schizophrenia from the premorbid to the postonset period, but the extent and developmental progression of decline varies across mental functions. 2 key findings →
Design: longitudinal study Participants: 1,037 Evidence: moderate
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MCI occurs often in this elderly Italian cohort and is associated with greater risk of AD, but only when the impairment involves the memory domain. 3 key findings →
Design: longitudinal study Participants: 1,016 Evidence: moderate
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Risk factors for progression from MCI to probable AD differed in men and women. 5 key findings →
Design: cohort study Participants: 294 Evidence: moderate
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Both cognitive impairment, no dementia and mild cognitive impairment are frequent in the Italian elderly (2,955,000 prevalent cases expected) and significantly predict progression to dementia. 3 key findings →
Design: longitudinal study 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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Identification of potentially modifiable risk factors for cognitive deterioration is important. 5 key findings →
Participants: 5,607 Evidence: low
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The incidence of CIND is greater than the incidence of dementia, and those with CIND are at high risk of progressing to dementia, making CIND a potentially valuable target for treatments aimed at slowing cognitive decline. 1 key finding →
Participants: 456 Evidence: low
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Because it is a potentially modifiable metabolic state, with multiple peripheral and central targets for intervention, it may represent a target for alleviating parkinsonian symptoms and slowing progression to disability and dementia. © 2022 The Authors. 2 key findings →
Evidence: low
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The Petersen/Winblad criteria classified 34% of participants as having MCI while the Jak/Bondi criteria classified 24% as MCI. 3 key findings →
Participants: 58 Evidence: low
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Most dementias are preceded by mild cognitive impairment (MCI), a transitional clinical stage characterized by cognitive decline that does not yet significantly interfere with activities of daily living. 5 key findings →
Design: systematic review Evidence: high
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In men, increasing depressive symptoms were associated with significantly steeper rates of cognitive decline, as measured by global cognitive and functional outcomes, and with an increased risk of dementia compared to consistently low depressive symptoms. 5 key findings →
Design: longitudinal study Participants: 811 Evidence: moderate
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Mild cognitive impairment (MCI) is a significant and increasingly recognized problem in individuals with type 2 diabetes mellitus (T2DM). 2 key findings →
Design: prospective cohort Participants: 100 Evidence: moderate
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Age, apolipoprotein E ε4 (APOE) and chromosomal sex are well-established risk factors for late-onset Alzheimer's disease (LOAD; AD). 1 key finding →
Evidence: low
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= 0.005). Cox regression analysis revealed that polypharmacy was significantly associated with a reduced risk of MCI progression to dementia (hazard ratio [HR] = 0.49, 95% confidence interval [CI]: 0.31 to 0.78) after adjusting for covariates. 5 key findings →
Design: cohort study Evidence: moderate
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Data point to a role for midlife vascular risk factors in the development of MCI in late life.
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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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% 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 →
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