Anti-amyloid therapies (AATs), such as anti-amyloid monoclonal antibodies, are emerging treatments for people with early Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Antibody-mediated removal of aggregated β-amyloid (Aβ) is the current, most clinically advanced potential disease-modifying treatment approach for Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Selecting the right dose is a significant challenge in designing clinical development programs, especially for slowly progressing diseases lacking predictive biomarkers of efficacy that may require long-term treatment to assess clinical benefit. 2 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Epilepsy is a cause of profound disability in patients with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Clinicaltrials.gov database demonstrates that relatively few clinical trials are undertaken for AD therapeutics, considering the magnitude of the problem. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The approvals of the first anti-amyloid antibodies for the treatment of Alzheimer's disease have changed both the clinical and research landscape for the disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Symptom-oriented treatment has been the mainstay of Alzheimer disease (AD) pharmacotherapy for decades. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Advances in amyloid targeting therapies (ATT) for Alzheimer's disease have introduced new options, necessitating an understanding of physicians' perspectives as these therapies move from trials to practice. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
On 22 May 2025, the Therapeutic Goods Administration (TGA) announced that the anti-amyloid monoclonal antibody donanemab (Eli Lilly, Kisunla) was approved in Australia for the treatment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This Editorial reviews data on the efficacy and adverse effects of lecanemab amongst individuals with mild Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid monoclonal antibodies (MABs) have introduced a new era of Alzheimer's disease (AD) therapeutics with disease-targeted drugs. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
We retrospectively reviewed 20 consecutive patients with Alzheimer's disease who switched from lecanemab to donanemab. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Based on "reducing amyloid plaques in the brain", the U.S. Food and Drug Administration has granted accelerated and full approval for two monoclonal anti-Alzheimer's antibodies, aducanumab and lecanemab, respectively. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia, which is characterized by a progressive neurodegenerative disorder that is extremely difficult to treat and severely reduces quality of life. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Solanezumab produced statistically significant increases in CSF total Aβ isoforms versus placebo, which correlated with CSF solanezumab concentration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder, and for providers the term AD is often avoided, favoring generic terms like memory loss or dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is the leading cause of dementia worldwide and a critical public health problem. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent rejection of lecanemab by the European Medicines Agency despite its approval in other countries highlights the debate among researchers and regulatory bodies about the efficacy, safety, and underlying scientific basis of drugs to treat Alzheimer’s disease. [Image: see text] 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Donanemab is a humanized monoclonal antibody that significantly reduces cerebral amyloid plaques in Alzheimer's Disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a major cause of dementia, that affects approximately 7-8% of people aged 65 years and older (according to WHO & Alzheimer's Disease International) and thus is a major concern in public health world-wide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The approval of lecanemab by the US Food and Drug Administration has been touted as a defining moment in the treatment of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The introduction of anti-amyloid antibodies has ushered in a new era in the treatment of Alzheimer's disease (AD), coinciding with the revision of its diagnostic criteria, which now focus on the biological definition of AD, with amyloid beta at its core. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid cascade hypothesis for Alzheimer's disease is still alive, although heavily challenged. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
CAA-ri gains increasing interest as a spontaneous human model of iatrogenic edematous amyloid-related imaging abnormalities (ARIA-E) in the context of amyloid-modifying therapies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 333 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Biomarker treatment effects in two phase 3 trials of gantenerumab
- Impact of Anti-amyloid-β Monoclonal Antibodies on the Pathology and Clinical Profile of Alzheimer's Disease: A Focus on Aducanumab and Lecanemab
- P4–285: SAR228810: An antiprotofibrillar beta‐amyloid antibody designed to reduce risk of amyloid‐related imaging abnormalities (ARIA)
- Amyloid-Related Imaging Abnormality (ARIA) Beyond the APOE-ε4 Allele
- The Impact of Anti-Amyloid Immunotherapies on Stroke Care
- Donanemab: Not two without a third
- Initial Experiences with Amyloid-Related Imaging Abnormalities in Patients Receiving Aducanumab Following Accelerated Approval
- First administration of the Fc-attenuated anti-β amyloid antibody GSK933776 to patients with mild Alzheimer's disease: a randomized, placebo-controlled study
- Amyloid-related imaging abnormalities-haemosiderin (ARIA-H) in patients with Alzheimer's disease treated with bapineuzumab: a historical, prospective secondary analysis
- Quantitative systems pharmacology-based exploration of relevant anti-amyloid therapy challenges in clinical practice
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 →