Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

Showing 26–50 of 135 studies with an author at Instituto de Salud Carlos III (ES) (page 2 of 6) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 135 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.

The regulation of vasculature is a prominent causal component of probable AD. 3 key findings →

Design: meta-analysis Evidence: high

A rare coding variant (rs72824905, p.P522R) conferring protection against Alzheimer's disease (AD) was identified in the gene encoding the enzyme phospholipase-C-γ2 (PLCG2) that is highly expressed in microglia. 4 key findings →

Design: longitudinal study Participants: 10,097 Evidence: moderate

In this cohort study, high adherence to a flavonoid-rich diet score was associated with a lower risk of dementia, with reductions more pronounced in individuals with a high genetic risk, hypertension, and depressive symptoms. 5 key findings →

Design: cohort Participants: 121,986 Evidence: moderate

New insights into the genetic etiology of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Nature genetics 2022-04-04

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →

Evidence: low

Higher adherence to the MedDiet was associated with greater gut microbial diversity (p < 0.05) and distinct microbial composition (PERMANOVA, p = 0.001). 5 key findings →

Design: longitudinal study Participants: 746 Evidence: moderate

The effect of Lewy body (co-)pathology on the clinical and imaging phenotype of amnestic patients

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Brain 2025-01-31

Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68). 5 key findings →

Design: longitudinal study Participants: 661 Evidence: moderate

After 12 months, no statistically significant difference was observed between MLI+EGCG and MLI+placebo in the PACC-exe (adjusted mean difference [AMD]: 0.12; 95%CI: -0.01, 0.24; p=0.061). 4 key findings →

Participants: 129 Evidence: high

Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. 3 key findings →

Design: longitudinal study Evidence: moderate

DOPA Decarboxylase (DDC) has been proposed as a cerebrospinal fluid (CSF) biomarker with increased concentrations in Lewy body disorders (LBDs) and highest levels in patients receiving dopaminergic treatment. 2 key findings →

Design: longitudinal study Participants: 71 Evidence: moderate

Disease-modifying effects of TMEM106B in genetic frontotemporal dementia: a longitudinal GENFI study

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Brain 2025-04-22

Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →

Design: cohort study Participants: 518 Evidence: moderate

These findings on participants who are at high risk of dropout may be useful in the planning phase of future prospective studies. 4 key findings →

Design: longitudinal study Participants: 5,278 Evidence: moderate

A polygenic score (PGS) for Alzheimer's disease (AD) was derived recently from data on genome-wide significant loci in European ancestry populations. 4 key findings →

Design: cohort Evidence: high

Ageing and a sedentary lifestyle are associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning. 2 key findings →

Evidence: high

The 6-year absolute risk was 12.0% (95% CI, 11.9% to 12.1%) in the control group (349 cases) and 9.5% (CI, 9.4% to 9.5%) in the intervention group (280 cases). 5 key findings →

Participants: 4,746 Evidence: high

Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer's disease (AD) in Caucasians. 2 key findings →

Design: meta-analysis Evidence: high

The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →

Design: longitudinal study Participants: 350 Evidence: moderate

Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis. 4 key findings →

Participants: 3,350 Evidence: low

In 2018, Carlos et al. [2] reviewed 21 studies from the SUN project that focused on the association between the MDP and several incident chronic diseases, concluding that high Mediterranean diet adherence was associated with a lower incidence of all-cause mortality, cardiovascular disease, type 2 diabetes, weight gain, metabolic syndrome, depression, cognitive decline, and nephrolithiasis, and with a lower heart rate and mitigation of the effects of obesity on cardiovascular disease (CVD) and type 2 diabetes, and our results suggested that the Mediterranean diet may improve fertility. 5 key findings →

Design: cohort study Participants: 79 Evidence: moderate

The CITA GO-ON Study, as a part of the World-Wide FINGERS network, is designed to validate the efficacy of a multidomain lifestyle intervention for dementia prevention and contribute valuable data to inform public health strategies fostering healthy, active aging. 3 key findings →

Design: randomized controlled trial Participants: 1,051 Evidence: high

We have established a valuable homogeneous single-center cohort which, by identifying groups of variables associated with high risk of MCI or dementia conversion, should help to clarify the early physiopathological mechanisms of AD and should provide avenues for prompt diagnosis and AD prevention. 2 key findings →

Design: cohort study Participants: 1,169 Evidence: moderate

We included 394,255 individuals including 184 incident cases of CD and 459 of UC after median follow-up of 13.6 years (4,889,910 person-years). 5 key findings →

Participants: 394,255 Evidence: moderate

↑ Change the filters

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