Aducanumab is the first FDA-approved amyloid-lowering immunotherapy for Alzheimer's disease. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Monoclonal antibodies targeting amyloid-β are the first approved disease-modifying treatment for Alzheimer’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These same brain areas were then assessed in a cohort of patients with Alzheimer’s disease versus a healthy older reference group, using a region of interest approach combined with standard structural (MRI), metabolic (fluorodeoxyglucose-PET) and amyloid ligand (florbetapir-PET) neuroimaging. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Understanding the continuum between sARIA and dARIA is crucial for improving diagnostic criteria, risk stratification, and therapeutic approaches. 2 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Since the 2021 FDA approval of the first monoclonal antibody (MAB) therapy for Alzheimer's disease (AD), treatment has progressed from symptom management to targeting and reducing amyloid β plaque burden. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid monoclonal antibodies are the first drugs approved as disease targeted therapies for the treatment of early Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the European authorisation of lecanemab and donanemab, Italy is entering the era of disease-modifying therapy for early symptomatic Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Basement membrane components are integral to the physiologic function of cerebral microvessels. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monoclonal antibodies that target Aβ monomers, soluble oligomers and protofibrils, and insoluble fibrils/plaques were developed, and not all have provided clinical benefit. 4 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Multimodal neuroimaging plays an indispensable role in the diagnosis, monitoring, and therapeutic evaluation of monoclonal antibody (mAb) therapies for Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This paper reviews the required imaging protocols and criteria for patient eligibility and discusses the key findings of ARIA-E and ARIA-H. These findings should be detected and interpreted by the practicing radiologist to ensure patient safety. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
EXT showed high cross-sectional reliability and longitudinal stability. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the last 2 years, there have been 3 successful trials of antiamyloid antibodies in Alzheimer disease (AD): aducanemab, now controversially US Food and Drug Administration-approved under the accelerated approval pathway1; lecanemab, now FDA-approved2; and donanemab, now going through the approval process.3 All 3 share a common broad mechanism, that is, antibody-mediated removal of β-amyloid (Aβ) from the brain, and this is almost certainly the basis of their therapeutic action.4 When used in the earliest symptomatic stages of AD, all have modest clinical effects, all clear Aβ from the brain, and all show evidence for some changes in molecular markers believed to be downstream of Aβ accumulation in keeping with disease modification.4 However, all these drugs-and several other antiamyloid immunotherapies that failed to show positive effects in clinical trials (e.g. bapineuzemab and gantenerumab)5,6-have the troubling adverse event of antibody-related imaging abnormalities (ARIA). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab is a humanized monoclonal antibody that is selective for soluble amyloid-beta (Aβ) aggregates. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
45/100
Alzheimer's disease (AD) affects over 6 million people over the age of 65. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent advancements in Alzheimer's disease treatment have focused on the elimination of amyloid-beta (Aβ) plaque, a hallmark of the disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab (product name Leqembi®) is an anti-amyloid monoclonal antibody treatment approved for use in Korea for patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common cause of dementia in the elderly population (aged 65 years and over), followed by vascular dementia, Lewy body dementia, and rare types of neurodegenerative diseases, including frontotemporal dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by the accumulation of amyloid-beta (Aβ) and neurofibrillary tangles of hyperphosphorylated tau in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These guidelines facilitate the accurate diagnosis and effective management of ARIA; ensure the safe administration of anti-Aβ drugs; and provide a framework for MRI facilities, includes staffing requirements and the use of MRI management systems. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
The prevalence of cerebral amyloid angiopathy (CAA) has been shown to increase with age, with rates reported to be around 50-60% in individuals over 80 years old who have cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab is an anti-amyloid monoclonal antibody, recently approved in the UK as a treatment for mild cognitive impairment (MCI) and mild dementia due to Alzheimer's disease (AD) in adults who are apolipoprotein E ε4 gene (APOE4) heterozygotes or non-carriers.A group of UK neurologists, old age psychiatrists and geriatricians with expertise in AD convened to agree appropriate use recommendations for lecanemab in UK clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, the leading cause of dementia, is defined by extracellular amyloid‑β (Aβ) plaques, intracellular tau aggregates and neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These guidelines facilitate the accurate diagnosis and effective management of ARIA; ensure the safe administration of anti-Aβ drugs; and provide a framework for MRI facilities, includes staffing requirements and the use of MRI management systems. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The introduction of anti-amyloid therapies for Alzheimer's disease (AD), such as lecanemab (Lequembi ® ), which was recently approved in Korea, necessitates careful monitoring for amyloid-related imaging abnormalities (ARIA) using brain MRI. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
- Randomized / 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
- Multicenter 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 Where this research is being discussed: events