Activated microglia may play a role in the pathogenesis of Alzheimer disease (AD) as they cluster around beta-amyloid (Abeta) plaques. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Activated microglia may play a role in the pathogenesis of Alzheimer disease (AD) as they cluster around beta-amyloid (Abeta) plaques. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) accounts for 60-70% of the population with dementia. 1 key finding →
Participants: 196 Evidence: low
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Significant interactions between amyloid status and modifiable risk factors were observed for diabetes (adjusted β = -0.206, p = 0.032), high cholesterol (adjusted β = -0.155, p < 0.001), and physical inactivity (adjusted β = -0.161, p = 0.046), indicating combined effects rather than additive effects on cognitive decline among Aβ+ individuals. 5 key findings →
Design: cohort study Participants: 1,707 Evidence: moderate
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BackgroundWith the changing demographic landscape in most countries worldwide, early identification of cognitive impairment in multicultural populations is increasingly relevant. 2 key findings →
Design: cross-sectional Participants: 187 Evidence: low
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According to the results, 31.4% of the sample consisted of subjects without cognitive impairment, 40.5% were identified as possible cases of MCI, and 24.9% as possible cases of dementia. 5 key findings →
Design: cross-sectional Participants: 385 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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P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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Parkinson's disease (PD) is a neurodegenerative condition that may affect both motor and cognitive function. 1 key finding →
Design: longitudinal study Participants: 115 Evidence: moderate
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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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Accurate prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is critical for early intervention. 1 key finding →
Design: longitudinal study Participants: 596 Evidence: moderate
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From the 144 participants (56.3% female and 43.7% male, with a mean [standard deviation] age of 80.7 [7.7] years), 118 participants were available for final follow-up. 4 key findings →
Design: cohort study Participants: 144 Evidence: moderate
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Utilizing [18F]-AV-1451 tau positron emission tomography (PET) as an Alzheimer disease (AD) biomarker will require identification of brain regions that are most important in detecting elevated tau pathology in preclinical AD. 1 key finding →
Evidence: moderate
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As one of the first attempts to use an imaging technique that does not require amyloid-specific radioligands for identification of individuals with brain amyloidosis, our findings could lead to development of multidisciplinary/multimodality brain amyloidosis biomarkers that are reliable, minimally invasive, and widely available. 3 key findings →
Participants: 62 Evidence: moderate
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Defective mitophagy is consistently found in postmortem brain and iPSC-derived neurons from Alzheimer disease (AD) patients. 1 key finding →
Participants: 100 Evidence: low
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Conventional MCI criteria were insufficient to allow for the creation of well-defined and internationally comparable samples of MCI patients. 1 key finding →
Design: cohort study Participants: 395 Evidence: high
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People with MCI are at increased risk of developing AD. 5 key findings →
Design: systematic review Participants: 51 Evidence: high
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Mild cognitive impairment and mild dementia are common problems in the elderly. 5 key findings →
Evidence: low
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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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Incorporating quantitative assessment of learning ability along with vMRI or CSF biomarkers in the clinical workup of MCI can provide critical information on risk of imminent conversion to AD. 3 key findings →
Evidence: low
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Rates of atrophy accelerate as individuals progress from amnestic mild cognitive impairment (aMCI) to typical late onset Alzheimer disease (AD). 1 key finding →
Participants: 46 Evidence: low
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We found no evidence of acceleration in whole-brain atrophy rates in any group. 1 key finding →
Evidence: low
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The AS task is a useful measure of executive function across the AD spectrum. 1 key finding →
Participants: 182 Evidence: low
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MicroRNAs (miRNAs) are small regulatory RNAs that participate in posttranscriptional gene regulation in a sequence-specific manner. 3 key findings →
Evidence: low
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Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
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Spatial patterns of brain atrophy in mild cognitive impairment (MCI) and Alzheimer's disease (AD) were measured via methods of computational neuroanatomy. 3 key findings →
Evidence: moderate
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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.
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events