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Find studies

Showing 301–325 of 701 studies in Mild cognitive impairment (page 13 of 29) · 27,780 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.

Subjective cognitive complaints are a criterion for the diagnosis of mild cognitive impairment (MCI), despite their uncertain relationship to objective memory performance in MCI. 4 key findings →

Evidence: moderate

Predicting Alzheimer's disease (AD) in individuals with some symptoms of cognitive decline may have great influence on treatment choice and disease progression. 4 key findings →

Evidence: low

Given the increased risk of progression to dementia for those identified as having MCI, the role of awareness should be explored further with due consideration given to the conceptualization of awareness and the methodology employed. 4 key findings →

Evidence: low

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

Plasma microRNA biomarkers for detection of mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Aging 2012-09-01

Early stages of many neurodegenerative diseases, such as Alzheimer's disease, vascular and frontotemporal dementia, and Parkinson's disease, are frequently associated with Mild Cognitive Impairment (MCI). 2 key findings →

Design: longitudinal study Evidence: moderate

Cognitive decline in older adults contributes to reduced ability to perform daily tasks and continued disuse leads to muscle weakness and potentiates functional loss. 1 key finding →

Design: longitudinal study Evidence: moderate

These findings suggest that neuropsychiatric symptoms in MCI are a predictor of progression to AD. 4 key findings →

Participants: 39 Evidence: low

Retinal nerve fiber layer thickness (RNFL) measured by means of Optical Coherence Tomography (OCT) has been used as a marker not only of ophthalmologic diseases but also of neurodegenerative diseases such as Alzheimer's disease (AD) and mild cognitive impairment (MCI). 1 key finding →

Design: cross-sectional Participants: 18 Evidence: low

Rich club disturbances of the human connectome from subjective cognitive decline to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Theranostics 2018-05-11

We demonstrated that rich club organization was disrupted, with reduced structural connectivity among rich club nodes, in aMCI and d-AD patients but remained stable in SCD patients. 5 key findings →

Participants: 62 Evidence: low

Optical Coherence Tomography in Alzheimer's Disease and Other Neurodegenerative Diseases

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Frontiers in neurology 2017-12-19

Over the past decade, a surge of evidence has documented various pathological processes in the retina of patients suffering from mild cognitive impairment, Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative diseases. 1 key finding →

Design: cross-sectional Evidence: low

MRI and CSF studies in the early diagnosis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of internal medicine 2004-09-01

In cross-section and longitudinally, our results show that evaluations of the P-tau231 level are highly correlated with reductions in the MRI hippocampal volume and by using CSF and MRI measures together one improves the separation of NL and MCI. 5 key findings →

Design: cross-sectional Evidence: moderate

Emotional changes are common in mild cognitive impairment (MCI) and Alzheimer's disease (AD). 5 key findings →

Participants: 237 Evidence: low

Characterizing Alzheimer's disease using a hypometabolic convergence index

✓ Peer-reviewed alzhub usefulness score 51 out of 100. NeuroImage 2011-01-27

This article introduces a hypometabolic convergence index (HCI) for the assessment of Alzheimer's disease (AD); compares it to other biological, cognitive and clinical measures; and demonstrates its promise to predict clinical decline in mild cognitive impairment (MCI) patients using data from the AD Neuroimaging Initiative (ADNI). 2 key findings →

Evidence: low

Executive predominant AD may reflect an alternative underlying pathophysiology related to genetic status, reflected in more prominent pathological alterations in frontoparietal regions subserving executive function. 2 key findings →

Participants: 100 Evidence: low

Pattern of regional cortical thinning associated with cognitive deterioration in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. PloS one 2013-01-24

The pattern of regional decreased cortical thickness that relates to cognitive deterioration is present in PD-MCI patients, involving areas that play a central role in the storage of prior experiences, integration of external perceptions, and semantic processing. 2 key findings →

Participants: 26 Evidence: low

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

This study aims to identify depressive risks in elderly individuals with subjective cognitive decline (SCD) and develop a predictive model using machine learning algorithms to enable timely interventions. 3 key findings →

Design: longitudinal study Evidence: moderate

The prominent prognostic role of carotid plaques in Aβ-negative MCI underscores the vascular contributions to non-amyloid cognitive decline and highlights the importance of evaluating both AD-related and vascular mechanisms in prodromal dementia. 1 key finding →

Design: longitudinal study Participants: 58 Evidence: moderate

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

• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD. 4 key findings →

Design: longitudinal study Participants: 1,051 Evidence: moderate

AI-powered model for accurate prediction of MCI-to-AD progression

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta Pharmaceutica Sinica B 2025-02-10

Alzheimer's disease (AD) remains a formidable challenge in modern healthcare, necessitating innovative approaches for its early detection and intervention. 2 key findings →

Design: longitudinal study Evidence: moderate

The National Institute on Aging and the Alzheimer’s Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer’s disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →

Evidence: low

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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. Show only studies that are free to read

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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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 →

Newest studies, as a dated timeline →    Atom feed