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Find studies

Showing 1–25 of 58 studies in Drug development scoring ≤ 29 out of 100 (page 1 of 3) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Drug development” covers

Drug development — Candidate treatments on their way through the pipeline, from the laboratory to early human trials.

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 Medicolegal and Ethical Dimensions of Physician Prescription Reluctance

✓ Peer-reviewed alzhub usefulness score 28 out of 100. Continuum (Minneapolis, Minn.) 2022-06-01

This article addresses the potential legal ramifications for neurologists caring for patients with Alzheimer disease (AD) who elect neither to prescribe aducanumab nor to refer patients with AD for treatment with aducanumab. 4 key findings →

Evidence: low

Our findings reveal various concerns about Aduhelm involving efficacy, safety, and affordability. 4 key findings →

Evidence: low

Etiology, risk factors, treatments and current status of Alzheimer's disease in Mexico

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Gaceta medica de Mexico 2022-01-01

Alzheimer's disease is a neurodegenerative disorder whose etiology continues to be discussed, to the point that there are different hypotheses that seek to clarify it, in addition to the fact that, given its multifactorial nature, there are different risk factors associated with its development. 4 key findings →

Evidence: low

[Aducanumab and Alzheimer's disease: a critical reflection.]

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Recenti progressi in medicina 2021-07-01

On June 7, 2021, the US Food and Drug Administration (FDA) approved aducanumab, a monoclonal amyloid targeting β-amyloid, for the treatment for Alzheimer's disease (AD). 4 key findings →

Design: clinical trial Evidence: low

Various medicinal agents aimed at improving Alzheimer disease (AD) include cholinesterase inhibitors, memantine, aducanumab, and antioxidants. 3 key findings →

Evidence: low

[Alzheimer's disease-Which substances are at present in phase III studies?]

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Der Nervenarzt 2022-03-14

The recent approval of aduhelm/aducanumab by the US Food and Drug Administration (FDA) in June 2021 raised hopes that further substances against Alzheimer's disease might be approved in the near future. 4 key findings →

Evidence: low

Aducanumab Use in Symptomatic Alzheimer Disease Evidence in Focus [RETIRED]: A Report of the AAN Guidelines Subcommittee

⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Neurology 2022-02-23

The author panel systematically reviewed available clinical trial data detailing aducanumab use in individuals with early symptomatic Alzheimer disease. 4 key findings →

Design: clinical trial Evidence: low

Education and Alzheimer Disease Genetic Risk in Associations of GLP-1 Receptor Agonists With Dementia Among Adults With Type 2 Diabetes

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-08

We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →

Design: cohort study Participants: 14,364 Evidence: moderate

Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer disease brain

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2025-05-21

Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). 4 key findings →

Design: cross-sectional Evidence: low

Exploring Natural Compounds for Alzheimer's Disease: Virtual Screening and Docking Study with KIBRA Protein

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2024-02-05

Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer. 4 key findings →

Evidence: low

Recent clinical and epidemiological studies support the contention that diabetes mellitus (DM) is a strong risk factor for the development of Alzheimer's disease (AD). 3 key findings →

Evidence: low

Tryptanthrin Analogs Substoichiometrically Inhibit Seeded and Unseeded Tau4RD Aggregation

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2024-02-03

Microtubule-associated protein tau is an intrinsically disordered protein (IDP) that forms characteristic fibrillar aggregates in several diseases, the most well-known of which is Alzheimer's disease (AD). 5 key findings →

Evidence: low

Progranulin deficiency promotes neuroinflammation through cathepsin B-mediated activation of the NLRP3 inflammasome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13

Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →

Evidence: low

Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 2 key findings →

Evidence: low

Alzheimer's Disease as the Result of Aberrant Reactivation of Embryonic Brain Pathways Silenced Decades Earlier

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-22

These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses. 3 key findings →

Evidence: moderate

Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression. 2 key findings →

Evidence: low

The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer’s disease (AD) and Down Syndrome (DS). 3 key findings →

Evidence: low

Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →

Evidence: low

Conformation-based detection of tau seeds with a novel VHH

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-12-08

In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →

Evidence: low

Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →

Design: cross-sectional Participants: 2,523 Evidence: moderate

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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