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Find studies

Showing 26–50 of 53 studies by Vellas B (page 2 of 3) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 53 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.

Entorhinal cortex thickness predicts cognitive decline in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Journal of Alzheimer's disease : JAD 2013-01-01

Biomarkers for Alzheimer's disease (AD) based on non-invasive methods are highly desirable for diagnosis, disease progression, and monitoring therapeutics. 4 key findings →

Design: longitudinal study Evidence: moderate

The European Union AddNeuroMed program and the US-based Alzheimer Disease Neuroimaging Initiative (ADNI) are two large multi-center initiatives designed to collect and validate biomarker data for Alzheimer's disease (AD). 5 key findings →

Participants: 1,074 Evidence: moderate

Vitality was associated with disability primarily through the mediation of other IC domains. 2 key findings →

Design: longitudinal study Participants: 1,389 Evidence: moderate

Defining the primary cognitive endpoint is a major decision for Alzheimer's disease preventive trials. 1 key finding →

Design: randomized controlled trial Evidence: high

Persons with dementia suffer different losses at different stages of the disease and therefore accurate assessment of abilities and losses is critical to assist the person in planning for their future and for care needs. 1 key finding →

Design: randomized controlled trial Evidence: high

A study with a more intensive multidomain intervention might bring further insights on this topic. 3 key findings →

Participants: 1,679 Evidence: high

Brain amyloid-beta (Aβ) plaques, a hallmark of the pathophysiology of Alzheimer's disease, have been associated with frailty. 4 key findings →

Participants: 477 Evidence: low

The MAPT Study is the first preventive trial involving multidomain interventions. 2 key findings →

Participants: 300 Evidence: high

In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. 4 key findings →

Participants: 58 Evidence: low

The CDR-SB assesses both cognitive and functional domains of AD disability. 4 key findings →

Participants: 382 Evidence: low

It is unknown whether multidomain interventions, which might preserve late-life cognition, affect Alzheimer's disease pathology. 4 key findings →

Participants: 527 Evidence: high

Mild cognitive impairment (MCI) was proposed as a nosological entity referring to elderly people with mild cognitive deficit but no dementia. 1 key finding →

Evidence: low

The secreted peptide adropin is highly expressed in human brain tissues and correlates with RNA and proteomic risk indicators for dementia. 2 key findings →

Participants: 452 Evidence: low

Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks. 4 key findings →

Evidence: low

Intrinsic capacity (IC) is a recent key concept proposed by the World Health Organization (WHO) based on aspects of functional ability (both physical and mental) rather than the presence or absence of diseases, with a potential to predict several health outcomes. 4 key findings →

Design: cross-sectional Participants: 491 Evidence: low

This study failed to find associations of circulating NfL and PGRN levels with frailty among community-dwelling older adults in adjusted analyses. 2 key findings →

Design: cross-sectional Participants: 403 Evidence: low

This review highlights a great heterogeneity in RCTs design of drugs for A/A in AD and some key methodological issues such as definition of A/A, choice of outcome measures and caregiver participation that could be addressed by an expert consensus to optimize future trials design. 5 key findings →

Participants: 18 Evidence: high

Weight loss is a frequent complication of Alzheimer's disease (AD) and a strong predictor of adverse outcomes in patients suffering from this disease. 4 key findings →

Evidence: moderate

This study aims to assess the evolution of cognitive performances over a 5-year follow-up period in community-dwelling older people with negative plasma p-tau181 levels and to determine whether frailty could discriminate between those who experience cognitive decline and those who do not, in the p-tau negative groups. 4 key findings →

Design: longitudinal study Evidence: moderate

The AddNeuroMed and ADNI cohorts were combined giving a total of 329 healthy controls, 421 mild cognitive impairment patients, and 286 Alzheimer's disease (AD) patients. 4 key findings →

Participants: 329 Evidence: low

Reducing participant burden, while ensuring that technological tools are suitable for older individuals, maintaining face-to-face contacts, and taking into account participant characteristics may increase adherence in future trials. 1 key finding →

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