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Find studies

Showing 726–750 of 1,172 studies · free to read · tagged Early Stage (page 30 of 47) · 31,380 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.

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.

Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →

Evidence: low

A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →

Design: cross-sectional Evidence: low

Data from 17 107 individuals (321 Asian, 635 Black, 829 Hispanic, and 15 322 White) with MCI or dementia and amyloid PET were analyzed between April 2020 and January 2022. 5 key findings →

Design: cohort study Participants: 3,154 Evidence: moderate

ARTS is associated with vascular risk factors, MCI, dementia, and stroke

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Alzheimer s & Dementia 2025-06-30

Higher ARTS score was associated (all ps < 0.01) with incident MCI (hazard ratio [HR] = 1.29), dementia (HR = 1.33), and stroke (HR = 1.52) and with diastolic/systolic blood pressure, self-reported hypertension, claudication, congestive heart failure, smoking, and glomerular filtration rate in the combined sample. 5 key findings →

Participants: 707 Evidence: low

All groups showed significantly increased brain-PAD, and the median (IQR) brain-PAD was 4.3 (5.4) years in MCI, 6.3 (6.2) years in AD, and 5.0 (6.5) years in DLB. 4 key findings →

Design: cross-sectional Participants: 185 Evidence: low

Males were more likely than females to present with two or more core DLB clinical features 2 years prior to obtaining a diagnosis of dementia. 5 key findings →

Design: longitudinal study Evidence: moderate

Alzheimer’s disease (AD), a leading neurodegenerative disorder, progresses from an intermediary stage known as Mild Cognitive Impairment (MCI), characterized by measurable cognitive decline with retained functional independence. 1 key finding →

Design: longitudinal study Evidence: moderate

Detecting Alzheimer's disease (AD) in its earliest stages, particularly during an onset of Mild Cognitive Impairment (MCI), remains challenging due to the overlap of initial symptoms with normal aging processes. 3 key findings →

Participants: 78 Evidence: low

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

On the basis of the independent validation dataset, the 18 F-FDG PET model yielded a significantly higher predictive value than the amyloid PET model. 5 key findings →

Participants: 159 Evidence: low

Regional age-related atrophy after screening for preclinical alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurobiology of aging 2021-09-15

Brain atrophy occurs in aging even in the absence of dementia, but it is unclear to what extent this is due to undetected preclinical Alzheimer disease. 2 key findings →

Design: cross-sectional Evidence: moderate

β-Amyloid-Dependent and -Independent Genetic Pathways Regulating CSF Tau Biomarkers in Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurology 2022-08-01

Genetic pathways implicated in causing AD are related to altered levels of soluble tau through both Aβ-dependent and Aβ-independent mechanisms, which may have relevance for anti-tau drug development. 3 key findings →

Participants: 751 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 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.

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 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