Dementia is a leading cause of death and disability worldwide. 3 key findings →
Design: RCT Participants: 33,995 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The purpose of this systematic review and meta-analysis was to evaluate the performance of cerebrospinal fluid (CSF) beta amyloid 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) as potential diagnostic biomarkers for idiopathic normal-pressure hydrocephalus (iNPH) and to assess their utility indistinguishing patients with iNPH from those with Alzheimer disease (AD) and healthy normal controls. 4 key findings →
Design: systematic review Participants: 413 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among our participants, aMCI and VCIND demonstrated prevalence of 14.83% and 2.71%, respectively, and annual incidence (per 1000 person-years) of 69.6 and 10.6, respectively. 5 key findings →
Design: longitudinal study Participants: 2,051 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This disease is associated with numerous restrictions for those affected but also for caregivers and society. 2 key findings →
Design: randomized controlled trial Participants: 200 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
With the advancement of anti-amyloid treatments for Alzheimer disease, accurate assays for amyloid-β (Aβ) pathology are essential. 1 key finding →
Design: cross-sectional Participants: 431 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 209,468 decedents, 95,594 were selected after matching. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
51/100
Alzheimer's disease (AD) accounts for 60%-70% of all dementia cases, and clinical diagnosis at its early stage is extremely difficult. 2 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Subjects Naive mice, H4 human neuroglioma cells, and H4 human neuroglioma cells stably transfected to express full-length amyloid precursor protein. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Thirty-three studies were included. Over half were conducted in Western countries (n =20). 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD), the leading cause of senile dementia, lacks effective therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
Alpha-synuclein (aSyn) post-translational modifications (PTM), especially phosphorylation at serine 129 and C-terminal truncations, are highly enriched in Lewy bodies (LB), Lewy neurites, and other pathological aggregates in Parkinson's disease and synucleinopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies have suggested that children undergoing surgery under anesthesia could be at an increased risk for the development of learning disabilities, but whether anesthetics contribute to this learning disability is unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), characterized by the β-amyloid protein (Aβ) deposition and tau hyperphosphorylation, is the most common dementia with uncertain etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
42/100
Parkinson's disease (PD) is a progressive neurodegenerative disorder with a growing global burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prior work has shown that iron interacts with hyperphosphorylated tau, which contributes to the formation of neurofibrillary tangles (NFTs) in Alzheimer's disease (AD), whereas iron chelator desferrioxamine (DFO) slows down the clinical progression of the cognitive decline associated with this disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Eighteen studies identified four core components of multidomain interventions: physical exercise, cognitive training, nutrition, and cardiovascular risk management. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
OSA components are positively associated with the risk of ADRD. 5 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
Alzheimer’s disease (AD), the most prevalent form of dementia in the elderly, involves critical changes such as reduced aerobic glycolysis in astrocytes and increased neuronal apoptosis, both of which are significant in the disease’s pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Epidemiological studies have reported that highly fluoridated drinking water may significantly decrease the Intelligence Quotient (IQ) of exposed children. 4 key findings →
Evidence: low
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 →