Both act by binding with fibrillary conformations of Aβ plaques in the brain. 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.
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
A century ago, German neurologist Alois Alzheimer documented the first case of Alzheimer's disease (AD), illuminating cognitive impairments associated with the presence of abnormal protein clusters, including amyloid plaques and tau tangles, within the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) research has entered a new era with the recent positive phase 3 clinical trials of the anti-Aβ antibodies lecanemab and donanemab. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA) are adverse events reported in Alzheimer's disease trials of anti-amyloid beta (Aβ) therapies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All recently approved monoclonal antibodies (eg, aducanumab, lecanemab, and donanemab) for Alzheimer disease (AD) were shown to increase the risks of amyloid-related imaging abnormalities (ARIA) in randomized clinical trials, which can include brain swelling or hemorrhage. 4 key findings →
Participants: 240 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A total of 143 patients with cognitive concerns were included who underwent a PrecivityAD2 test as part of their clinical evaluation. 5 key findings →
Participants: 4,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Although β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
RESUMO A Doença de Alzheimer (DA) é uma condição progressiva caracterizada pelo acúmulo de placas de beta-amiloide e emaranhados neurofibrilares de proteína tau, resultando em perda sináptica e morte neuronal. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 4 of 5 patients treated with lecanemab or donanemab and who had moderate or severe ARIA-E, Aβ PET signal decreased significantly more in regions that had been involved with ARIA-E. Greater regional Aβ PET signal reduction in areas involved by ARIA-E may reflect enhanced local Aβ clearance, reduced tracer binding site availability, impaired glymphatic flow from immune complex deposition, or other mechanisms. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The blood-brain barrier (BBB) displays a highly organized and complex structure, which is important for maintaining brain homeostasis and protecting the brain from foreign molecules or pathogens. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early diagnosis of mild cognitive impairment (MCI) and Alzheimer's disease (AD) with mild dementia is becoming increasingly important to enable patients to receive appropriate treatment with available amyloid-targeting therapies. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid monoclonal antibodies (lecanemab and donanemab) represent the first disease-modifying therapies for early symptomatic Alzheimer's disease (AD)- Italy's National Health Service (SSN) must determine whether to include these therapies within Essential Levels of Care (LEA), requiring reimbursement across all regions. 5 key findings →
Participants: 42,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer Disease (AD) constitutes a major global healthcare problem. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab reduced clinical decline by roughly 27% over placebo, with ARIA-E in 12.6% of treated patients;donanemab slowed decline by about 35%, with ARIA-E near 24%. 4 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
PFT is longer at CDR-SB ≤ 2.0 (1-2 years) and shorter at CDR-SB ≥ 5 (≤ 0.33) in the Alzheimer's Disease Neuroimaging Initiative cohort. 5 key findings →
Design: open-label trial Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurodegenerative disease that imposes economic and societal burden. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Recent findings There is an association, but Alzheimer pathology explains less than 40% of the attributable risk of dementia when other pathologies such as vascular, Lewy Body and TDP-43 are accounted. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The study includes symptomatic DIAD participants and asymptomatic mutation carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-targeting antibody therapies for Alzheimer's disease require substantial diagnostic infrastructure including amyloid PET imaging, repeated MRI monitoring, and specialized clinical evaluation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Monoclonal antibodies targeting amyloid-β are the first disease-modifying treatments for Alzheimer disease to have received FDA-approval. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Neuroinflammation, mediated by activated microglia and astrocytes, exacerbates Aβ and tau pathology, contributing to synaptic loss and neuronal death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Anti-amyloid treatment (AAT) with monoclonal antibodies represents a major therapeutic advance in early Alzheimer disease (AD), but its introduction has important and underappreciated implications for vascular neurology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the pivotal study in the overall population, the treatment showed a difference of −0.45 points between lecanemab and placebo in the adjusted mean change from baseline on the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) at 18 months (the primary endpoint). 5 key findings →
Design: clinical trial Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →