27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synthesis methods We meta-analysed results for each outcome within each comparison using the inverse variance method and the random-effects model. 5 key findings →
Design: meta-analysis Participants: 20,342 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included. 3 key findings →
Design: cross-sectional Participants: 838 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The clinical diagnosis of synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), is challenging, especially at an early disease stage, due to the heterogeneous and often non-specific clinical manifestations. 5 key findings →
Participants: 18 Evidence: moderate
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Among 12,327 patients who underwent randomization (6162 to the asundexian group and 6165 to the placebo group), the incidence of ischemic stroke was lower in the asundexian group than in the placebo group (6.2% vs. 8.4%; cause-specific hazard ratio, 0.74; 95% confidence interval [CI], 0.65 to 0.84; P<0.001). 5 key findings →
Design: clinical trial Participants: 12,327 Evidence: low
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Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly. 2 key findings →
Design: cohort Participants: 1,567 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Cognition-oriented treatments (COTs) are a group of non-pharmacological treatments aimed at maintaining or improving cognitive functioning. 1 key finding →
Design: systematic-review Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinical data alone poorly predicted phenoconversion in RBD due to synucleinopathy patients. 3 key findings →
Participants: 173 Evidence: low
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Plasma GFAP alone differentiates AD from FTD and neurodegenerative dementias from HC but with lower accuracy than p-tau181 and NfL. 3 key findings →
Participants: 59 Evidence: moderate
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Patients with isolated rapid-eye-movement sleep behaviour disorder (RBD) are commonly regarded as being in the early stages of a progressive neurodegenerative disease involving α-synuclein pathology, such as Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. 1 key finding →
Evidence: low
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Neurofilament light chain (NfL) and α-synuclein oligomeric seeds (α-syn-s) are promising biomarkers for patients with parkinsonism. 4 key findings →
Participants: 153 Evidence: low
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Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia that is characterized by loss of muscle atonia during REM sleep (known as REM sleep without atonia, or RSWA) and abnormal behaviours occurring during REM sleep, often as dream enactments that can cause injury. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The identification of biomarkers predicting the burden of brain alpha-synuclein (α-syn) pathology in vivo represents a research priority in Lewy body disease (LBD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the initial kindred of ten affected Italian individuals (mean age of disease onset 59·8 years [SD 8·7]), we detected significant linkage of Parkinson's disease to chromosome 14 and nominated LRP10 as the disease-causing gene. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In the cohort, 39.2% (67/171) tested positive by α-syn SAA. α-syn SAA positivity was more frequently detected alone than in combination with biomarkers of AD pathology (25.1% vs. 14.0%). α-syn SAA+ status was independently associated with higher odds of fluctuating cognition (OR 2.99, 95%CI 1.46–6.25, p = 0.012), visual hallucinations (OR 2.41, 95%CI 1.24–4.75, p = 0.027), extrapyramidal signs (OR 4.57, 95%CI 2.35–9.11, p < 0.001) and akinetic mutism (OR 3.77, 95%CI 1.22–12.82, p = 0.038). 5 key findings →
Participants: 171 Evidence: moderate
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Autosomal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN) is characterized by late onset (30-40 years old) cerebellar ataxia, sensory neuronal deafness, narcolepsy-cataplexy and dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prevalent LB- and AD-related neurodegenerative pathologies affect a significant proportion of iNPH patients and contribute to cognitive decline (both) and motor impairment (only LB pathology) but do not significantly influence the surgical outcome at 6 months. 5 key findings →
Evidence: moderate
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The final cohort comprised more than 3 million individuals, with a mean baseline age of 63–65 years and a female proportion of 52–55%. 4 key findings →
Design: cohort study Evidence: moderate
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This joint Position Paper, developed by the Italian Expert Panel on Alzheimer convened by the Italian Society of Neurology with participation from multiple scientific societies, outlines strategic guidelines for reorganizing the patient journey in the era of anti-amyloid monoclonal antibodies for Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the whole sample, both PRSs were associated with the strength of correlation between GMV and different serotonin receptors and fluorodopa uptake. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer-Perusini's disease (AD) represents a growing health crisis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
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.
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.
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 →