Alzheimer's disease (AD) is a public health priority for the 21st century. 5 key findings →
Design: meta-analysis Participants: 74,046 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The muscarinic receptor agonist xanomeline improved cognition in phase 2 trials in Alzheimer's disease and schizophrenia. 3 key findings →
Design: clinical trial Participants: 60 Evidence: high
Full summary, score breakdown and related studies → Original source
71/100
Polysomnography (PSG) studies of sleep changes in Alzheimer's disease (AD) have reported but not fully established the relationship between sleep disturbances and AD. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Depression is an accepted risk factor for dementia, but it is unclear if this relationship is causal. 3 key findings →
Design: longitudinal study Participants: 388 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In addition to apolipoprotein E (APOE), recent large genome-wide association studies (GWASs) have identified nine other genes/loci (CR1, BIN1, CLU, PICALM, MS4A4/MS4A6E, CD2AP, CD33, EPHA1 and ABCA7) for late-onset Alzheimer's disease (LOAD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. 3 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source
66/100
Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. 3 key findings →
Design: longitudinal study Participants: 1,087 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Psychosis in Alzheimer's disease (AD) represents a distinct disease subtype with a more rapid progression of illness evidenced by an increased velocity of cognitive decline and a hastened mortality. 2 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and the most common form of dementia in the elderly. 2 key findings →
Design: case-control study Participants: 931 Evidence: moderate
Full summary, score breakdown and related studies → Original source
62/100
Previous animal models and structural imaging investigations have linked hippocampal neuroplasticity to electroconvulsive therapy (ECT) response, but the relationship between changes in hippocampal volume and temporal coherence in the context of ECT response is unknown. 2 key findings →
Design: longitudinal study Participants: 19 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein, can be measured in blood samples, and has been associated with Alzheimer's disease (AD). 4 key findings →
Design: cross-sectional Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source
Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer's disease (AD) in Caucasians. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Design: longitudinal study Participants: 1,184 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The relationship between mild behavioral impairment (MBI) and Alzheimer's disease (AD) is intricate and still not well investigated. 4 key findings →
Design: longitudinal study Participants: 1,129 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We systematically compared structural imaging patterns of advanced brain aging (ABA) in the general-population, herein defined as significant deviation from typical BA to those found in Alzheimer disease (AD). 5 key findings →
Participants: 2,705 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
55/100
Cigarette smoking has been associated with dementia and dementia-related brain changes, notably gray matter (GM) volume atrophy. 3 key findings →
Participants: 698 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
55/100
Mild-cognitive impairment (MCI) occurs in up to one-fifth of individuals over the age of 65, with approximately a third of MCI individuals converting to dementia in later life. 2 key findings →
Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It is broadly acknowledged that the onset of dementia in Alzheimer's disease (AD) may be modifiable by the management of risk factors. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The relationship between sleep quality, neurofilament light chain (NFL), and cognitive impairment, including the potential effect of plasma NFL in this association, remains unclear. 3 key findings →
Design: longitudinal study Participants: 640 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Various plasma biomarkers for amyloid-β (Aβ) have shown high predictability of amyloid PET positivity. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD) serves as an initial symptom of preclinical Alzheimer's disease (AD). 4 key findings →
Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Depression predisposes to medical illnesses and advances biological aging indicated by shorter telomere length, accelerated brain aging and advanced epigenetic aging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases likely share common underlying pathobiology. 5 key findings →
Participants: 82,337 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 →