A sensitive marker for monitoring progression of early Alzheimer's disease would help to develop and test new therapeutic strategies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A sensitive marker for monitoring progression of early Alzheimer's disease would help to develop and test new therapeutic strategies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment in Parkinson's disease is an important predictor for the progression to PDD. 1 key finding →
Participants: 166 Evidence: moderate
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Recent research has shown an increased rate of conversion to dementia in subjects with mild cognitive impairment (MCI) compared to controls. 5 key findings →
Participants: 13 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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Mild cognitive impairment (MCI) is a clinical condition characterized by a decline in cognitive ability and progression of cognitive impairment. 3 key findings →
Participants: 239 Evidence: moderate
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Little is known about the dysbiosis of the gut microbiome in patients with mild cognitive impairment (MCI) potentially at risk for the development of Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Participants: 14 Evidence: moderate
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< 0.001). Receiver operating characteristic (ROC) analysis identified right hippocampal MD and t-tau as optimal classifiers for AD. 4 key findings →
Design: cross-sectional Evidence: low
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Key markers and mechanisms were identified for each stage: initial neurophysiological deficits in SCD with compensatory metabolomic responses, gut-brain axis dysregulation in MCI, and extensive metabolic disruption and multisystem breakdown in AD. 5 key findings →
Participants: 277 Evidence: low
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We identified 8 brain structural features from 192 MRI features that were associated with the risk of MCI progressing to AD, including: left hippocampus, left inferior lateral ventricle, left amygdala, right middle temporal gyrus, left fusiform gyrus, right amygdala, left cortical total volume, and brain parenchyma total volume. 4 key findings →
Design: longitudinal study Participants: 947 Evidence: moderate
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Neurophysiological activity features and tau pet provided additional information to the clinical model when acquired up to ∼4 years prior to diagnosis, but their accuracy decreased at larger intervals. 5 key findings →
Design: longitudinal study Participants: 102 Evidence: moderate
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This innovative study aims to test the feasibility of iTBS as a cognitive enhancement strategy in MCI. 3 key findings →
Participants: 20 Evidence: high
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In amyloid PET–positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months. 2 key findings →
Design: cohort study Participants: 21 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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Controlling for baseline differences, 1 year of CPAP adherence in MCI +OSA significantly improved cognition, compared with a nonadherent control group, and may slow the trajectory of cognitive decline. 3 key findings →
Participants: 29 Evidence: low
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Mild cognitively impaired patients with memory plus other cognitive domain deficits, rather than those with pure amnestic MCI, constituted the high-risk group. 1 key finding →
Participants: 108 Evidence: low
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Chronic cerebral hypoperfusion has been associated with cognitive decline in aging and Alzheimer's disease. 3 key findings →
Evidence: low
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We investigated oxidative stress in human postmortem frontal cortexfrom individuals characterized as mild cognitive impairment (n= 8), mild/moderate Alzheimer disease (n = 4), and late-stage Alzheimer disease (n = 9). 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disease marked by deficits in episodic memory, working memory (WM), and executive function. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) refers to the transitional state between the cognitive changes of normal aging and very early dementia. 5 key findings →
Evidence: low
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Patients with MCI showed no significant difference (P>.05) in the number of diffuse plaques from that in normal controls or patients with EAD. 3 key findings →
Evidence: low
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The spectrum of cognitive decline in the elderly ranges from what can be classified as normal cognitive decline with aging to subjective cognitive impairment to mild cognitive impairment (MCI) to dementia. 4 key findings →
Evidence: low
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Animal studies have suggested that fine particulate matter (PM) can translocate from the upper respiratory tract to the brain and cause brain inflammation. 3 key findings →
Evidence: low
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Oxidative stress has been associated with the onset and progression of mild cognitive impairment (MCI) and Alzheimer disease (AD). 2 key findings →
Evidence: low
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Dysfunction of cholinergic basal forebrain (CBF) neurons of the nucleus basalis (NB) is a cardinal feature of Alzheimer's disease (AD) and correlates with cognitive decline. 3 key findings →
Evidence: low
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To determine whether the medial temporal lobe is atrophic in subjects with mild cognitive impairment, and whether atrophy of this structure is a better predictor of dementia than memory dysfunction. 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 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 →