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Find studies

Showing 301–325 of 504 studies in Mild cognitive impairment · free to read (page 13 of 21) · 30,980 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Mild cognitive impairment” covers

Mild cognitive impairment — The stage between normal ageing and dementia: who progresses, who doesn't, and what predicts it.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

In the MCI+NPS group, the most frequently endorsed NPS was anxiety (46.2 %), the less prevalent NPS was euphoria/elation (1.44 %). 5 key findings →

Design: cross-sectional Participants: 376 Evidence: low

All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status. 5 key findings →

Design: longitudinal study Participants: 47 Evidence: moderate

Among 558 amnestic MCI participants (168 ChEI users), ChEI users exhibited higher risk of progression to AD dementia (hazard ratio = 1.77, 95% confidence interval: 1.15 to 2.73, p = 0.001). 5 key findings →

Design: longitudinal study Evidence: moderate

< 0.001). Shape features demonstrated the highest predictive accuracy for conversion, with areas under the curve of 0.891 at baseline and 0.898 at 2 years. 5 key findings →

Design: longitudinal study Participants: 180 Evidence: moderate

The PD-MCI nonreversion group had greater p-tau:amyloid beta and t-tau:amyloid beta ratios relative to the PD-MCI reversion group. 4 key findings →

Design: longitudinal study Participants: 430 Evidence: moderate

Thirteen studies were included (five guidelines, two clinical decisions, two systematic reviews, one meta-analysis, and three RCTs). 3 key findings →

Design: meta-analysis Evidence: high

Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques. 3 key findings →

Design: longitudinal study Participants: 127 Evidence: moderate

Mild cognitive impairment (MCI) is generally referred to the transitional zone between normal cognitive function and early dementia or clinically probable Alzheimer's disease (AD). 4 key findings →

Evidence: low

Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD). 1 key finding →

Evidence: low

Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Scientific reports 2016-10-17

Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E ε4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. 4 key findings →

Evidence: low

= 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

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

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

< 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

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

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

Time‐dependent biomarker accuracy in forecasting mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer s & Dementia 2025-12-01

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

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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Where “Free full text” comes from

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.

How the 0–100 score works — and why some entries are capped

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.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

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 30,980 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.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,042 records (3.4% of the library) are not peer-reviewed — 967 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