Alzheimer's disease (AD) is the leading cause of dementia, characterized by irreversible neuronal loss and progressive cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid related imaging abnormalities (ARIA) are the most significant risk associated with the use of anti-amyloid monoclonal antibodies (MAB) for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a growing public health concern in Asia, with an increasing prevalence driven by demographic shifts and rising life expectancy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identify a risk hierarchy for ARIA-H among anti-Aβ mAbs and link specific mAb biophysical properties-Aβ binding type, affinity for soluble oligomers, epitope specificity, Fc structure, and plaque clearance dynamics-directly to ARIA-H pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent advances in hereditary dementia research have clarified its molecular pathogenesis and clinical applications, with several advances already reaching implementation. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder, the treatment of which remains a major clinical challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid monoclonal antibodies provide disease-modifying treatment options for selected patients with early symptomatic Alzheimer disease, but introduce new challenges for acute stroke care. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the UK-indicated population, excluding APOE ε4 homozygotes reduced, but did not eliminate, ARIA risk with donanemab. 2 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source
Passive immunotherapy targeting amyloid-β (Aβ) has emerged as a major therapeutic strategy for Alzheimer's disease (AD), yet its clinical benefits remain modest and are frequently accompanied by vascular adverse events such as amyloid-related imaging abnormalities (ARIA). 1 key finding →
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
Despite the risks of ARIA and other adverse events, Donanemab-azbt represents a promising addition to AD therapy, offering the potential for improved outcomes in patients with early symptomatic disease and expanding the therapeutic options beyond traditional symptomatic treatments. 4 key findings →
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
Alzheimer's dementia is a progressive neurodegenerative disorder in which cognitive decline, neuropsychiatric symptoms, and functional dependence emerge from a long preclinical and prodromal phase. 4 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
We induced ARIA without significant cortical CAA pathology and identified regional differences with TNF inhibition including a potential benefit of treatment in the hippocampus and possible detriment to pathology in the cortex. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Herbal therapy demonstrated a significant improvement in cognition and memory, which were similar to the donepezil in patients with aMCI. 3 key findings →
Participants: 216 Evidence: high
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
Alzheimer's disease (AD) stands as the predominant form of dementia, presenting significant and escalating global challenges. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
Donanemab is an amyloid-targeting therapy that resulted in robust amyloid plaque reduction and slowed Alzheimer's disease (AD) progression compared with placebo in the phase II TRAILBLAZER-ALZ study (NCT03367403). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The targeting of amyloid-beta (Aβ) plaques therapeutically as one of the primary causes of Alzheimer's disease (AD) dementia has been an ongoing effort spanning decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study has established a significant link between CAA-Aβ antibody immune complex formation, immune activation and vascular damage leading to smooth muscle cell loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The emerging class of bispecific antibodies represents a significant advancement in Alzheimer's disease (AD) immunotherapy by addressing the limited brain concentrations achieved with conventional monoclonal antibodies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid mAbs consistently demonstrated robust amyloid clearance and modest slowing of clinical decline in early symptomatic AD. 5 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
The development of humanized IgG1 anti-amyloid monoclonal antibodies, such as lecanemab, provides a promising novel treatment pathway with potential disease-modifying effects for patients with early Alzheimer's disease (AD). 5 key findings →
Design: narrative review 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 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