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Find studies

Showing 51–75 of 504 studies in Mild cognitive impairment · free to read (page 3 of 21) · 30,580 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.

ADCOMS is proposed as new standard outcome for pAD and mild AD dementia trials, and is progressing in a CAMD-sponsored qualification process for use in registration trials of pAD. 3 key findings →

Design: longitudinal study Evidence: moderate

An algorithm-derived diagnosis of aMCI showed few sociodemographic associations but was consistently associated with higher disability and neuropsychiatric symptoms in addition to showing substantial variation in prevalence across LAMIC populations. 4 key findings →

Design: cross-sectional Participants: 15,376 Evidence: moderate

The best cluster solution found was based on orthostatic hypotension, mild cognitive impairment, rapid eye movement sleep behavior disorder (RBD), depression, anxiety, and Unified Parkinson's Disease Rating Scale Part II and Part III scores at baseline. 1 key finding →

Design: cohort study Participants: 113 Evidence: moderate

These studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design. 2 key findings →

Design: longitudinal study Evidence: moderate

Neurogranin as a Cerebrospinal Fluid Biomarker for Synaptic Loss in Symptomatic Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. JAMA neurology 2015-11-01

Baseline CSF levels of NGRN in patients with AD (median level, 2381 pg/mL [interquartile range, 1651-3416 pg/mL]) were higher than in cognitively normal participants (median level, 1712 pg/mL [interquartile range, 1206-2724 pg/mL]) (P = .04). 3 key findings →

Design: longitudinal study Participants: 163 Evidence: moderate

The MetS was associated with an increased incidence of MCI and progression to dementia. 4 key findings →

Design: longitudinal study Participants: 984 Evidence: moderate

Sex and age differences in atrophic rates: an ADNI study with n=1368 MRI scans

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurobiology of aging 2010-08-01

We set out to determine factors that influence the rate of brain atrophy in 1-year longitudinal magnetic resonance imaging (MRI) data. 1 key finding →

Design: longitudinal study Participants: 363 Evidence: moderate

See Coulthard and Knight (doi:10.1093/aww335) for a scientific commentary on this article. 1 key finding →

Design: longitudinal study Participants: 530 Evidence: moderate

In this longitudinal study, we included 396 cognitively normal to dementia subjects with 18 F-Florbetapir/ 18 F-Florbetaben-amyloid-PET, 18 F-Flortaucipir-tau-PET and ~ 2-year cognitive follow-up. 1 key finding →

Design: longitudinal study Participants: 396 Evidence: moderate

Inflammatory proteins in plasma are associated with severity of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. PloS one 2013-06-10

Markers of Alzheimer's disease (AD) are being widely sought with a number of studies suggesting blood measures of inflammatory proteins as putative biomarkers. 4 key findings →

Design: longitudinal study Participants: 350 Evidence: moderate

Regions with early signs of elevated amyloid β uptake were used to form an early, focal composite and compared to a commonly used global composite, in a separate validation sample. 3 key findings →

Design: longitudinal study Participants: 279 Evidence: moderate

Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Archives of neurology 2009-09-01

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

These results demonstrate an important role of clusterin in the pathogenesis of AD and suggest that alterations in amyloid chaperone proteins may be a biologically relevant peripheral signature of AD. 4 key findings →

Design: longitudinal study Evidence: moderate

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

The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. 1 key finding →

Design: longitudinal study Participants: 551 Evidence: moderate

Due to the growing number of older adults with cognitive impairment, it is essential to delay the onset and progression of cognitive decline and promote a healthy lifestyle. 1 key finding →

Design: systematic review Evidence: high

Plasma clusterin concentration is associated with longitudinal brain atrophy in mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 64 out of 100. NeuroImage 2011-07-28

Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). 5 key findings →

Design: longitudinal study Participants: 139 Evidence: moderate

We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods. 3 key findings →

Participants: 165 Evidence: low

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

Cross-sectional functional magnetic resonance imaging studies using a memory task in patients with mild cognitive impairment have produced discordant results, with some studies reporting increased hippocampal activity--consistent with findings in genetic at-risk populations--and other studies reporting decreased hippocampal activity, relative to normal controls. 3 key findings →

Design: cross-sectional Participants: 33 Evidence: moderate

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

Tensor-based morphometry can recover three-dimensional longitudinal brain changes over time by nonlinearly registering baseline to follow-up MRI scans of the same subject. 2 key findings →

Design: longitudinal study Participants: 20 Evidence: moderate

Adjusted estimates of MTA were associated with significantly increased risk of developing dementia within 3 years, suggesting that obtaining a magnetic resonance image during the evaluation of MCI may offer additional independent information about the risk of progression to dementia. 2 key findings →

Participants: 190 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.

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 30,580 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.

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 30,580 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 →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events