The amyloid cascade hypothesis is a useful framework for therapeutic development in Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
43/100
Donepezil has psychotropic properties, and pretreatment behaviors help predict patients' responses to treatment. 4 key findings →
Design: open-label trial Participants: 86 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
Amyloid-β (Aβ) plaques and neurofibrillary tangles containing phosphorylated tau protein are major hallmarks of Alzheimer's disease (AD). 1 key finding →
Design: clinical trial 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
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
Psychosis and agitation are among the most distressing neuropsychiatric symptoms (NPSs) of Alzheimer's disease (AD), linked to faster disease progression and earlier admission to nursing homes. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases represent the most common cause of dementia. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Three deaths have been reported related to treatment with lecanemab.6 Patients receiving DMT require frequent monitoring with MRI brain scans (four or more per year), as there is a high rate of clinically significant amyloid-related imaging abnormalities (ARIA), both brain oedema (ARIA-E) and macro- and microhaemorrhages (ARIA-H). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Ranolazine and metformin may be frequently co‐administered in subjects with chronic angina and co‐morbid type 2 diabetes mellitus (T2DM). 2 key findings →
Design: clinical trial Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
The concentration of 124 I-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and Aβ immunohistochemistry results. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
β-Site amyloid precursor protein cleaving enzyme1 (BACE1) is one of the key enzymes involved in the processing of the amyloid precursor protein (APP) and formation of amyloid β peptide (Aβ) species. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We conducted an open-label study designed to assess the effects of tacrine on behavioral changes in patients with Alzheimer's disease (AD). 4 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mild cognitive impairment in Parkinson's disease (PD-MCI) can affect several cognitive domains, including attention, working memory, executive functions, language, visuospatial skills, and episodic memory, resulting in a progressive reduction of autonomy and an increased risk of dementia. 1 key finding →
Design: clinical trial Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
41/100
Many insults, including trauma, ischemia, infection, inflammation, and neurodegeneration, result in irreversible damage to the central nervous system. 3 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among the elderly, the prevalence of Alzheimer's disease and multi-infarct dementia, as opposed to depression, increases steeply with age. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Progress in understanding the complexity of Alzheimer's disease informs the search for combination therapies that can successfully prevent or substantially slow the progression of the disease. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
41/100
RoCA classifies patients similarly to gold standard paper-based tests, with a receiver operating characteristic area under the curve of 0.81 (95% CI 0.67-0.91; P<.001). 5 key findings →
Design: open-label trial Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Upon activation, platelet alpha-granules' soluble contents are secreted and membrane-bound contents are translocated to the plasma membrane. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The results of the present study suggest that increased 18 F-THK5351 uptake might be a useful predictor of poor prognosis among Aβ- aMCI patients, which might be associated with increased neuroinflammation (ClinicalTrials.gov NCT02656498). 3 key findings →
Design: clinical trial Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mechanisms underlying blood-brain barrier (BBB) compromise in human immunodeficiency virus (HIV) infection and the ways in which BBB compromise might impair neurocognitive function remain poorly understood. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Aducanumab and BAN2401 showed significant efficacy on both clinical and biomarker outcomes; gantenerumab showed significant biomarker effects, with no clinical efficacy reported to date; and ALZ-801 showed significant clinical effects in the high-risk population of patients homozygous for the ε4 allele of apolipoprotein E gene (APOE4) and a dose-dependent preservation of hippocampal volume. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
(18)F-flutemetamol uptake can be readily quantified. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Aducanumab, a human-derived antibody targeting amyloid-β (Aβ), is in Phase 3 clinical trials for the treatment of Alzheimer's disease. 1 key finding →
Design: clinical trial 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
- 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 →