28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Long-term use of urate-lowering therapies (ULT) may reduce inflammaging and thus prevent cognitive decline during aging. 3 key findings →
Design: randomized controlled trial Participants: 51 Evidence: high
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Our findings elucidate the predictive values of environmental factors and comorbid conditions in identifying RBD patients at higher risk of phenoconversion. 4 key findings →
Participants: 319 Evidence: moderate
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White matter hyperintensities (WMHs) are neuroimaging markers widely interpreted as caused by cerebral small vessel disease, yet emerging evidence suggests that a subset may have a neurodegenerative etiology. 1 key finding →
Participants: 32,526 Evidence: moderate
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This study investigated amyotrophic lateral sclerosis, an adult-onset neurological disorder that leads to the degeneration of motor neurons and involves TDP-43 as a key component of ubiquitinated aggregates. 2 key findings →
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The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. 1 key finding →
Design: cohort Evidence: moderate
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With the increase in large multimodal cohorts and high-throughput technologies, the potential for discovering novel biomarkers is no longer limited by data set size. 5 key findings →
Evidence: moderate
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One of the most devastating nonmotor manifestations of PD is dementia. 3 key findings →
Design: cross-sectional Participants: 13 Evidence: low
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The patient was participating in an extended open-label trial of aducanumab when she was admitted to hospital for focal seizures and ARIA in 2 noncontiguous regions of the left frontal and occipital lobes. 4 key findings →
Design: longitudinal study Evidence: moderate
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This study suggests that the Intensive Care Delirium Screening Checklist can easily be applied by a clinician or a nurse in a busy critical care setting to screen all patients even when communication is compromised. 3 key findings →
Participants: 93 Evidence: low
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In this multi-cohort study of older adults without cognitive impairment, we show that WMH and lacunes independently predict increased risk of MCR, after adjusting for key confounders. 5 key findings →
Design: cohort study Participants: 1,772 Evidence: moderate
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Neurodegeneration occurring in multiple sclerosis (MS) contributes to the progression of disability. 4 key findings →
Evidence: low
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Cognitive impairment is a frequent feature of COPD. 4 key findings →
Design: longitudinal study Evidence: moderate
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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
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Data collection will begin in four Canadian provinces (Alberta, Manitoba, Ontario and Saskatchewan) in February 2020 and is expected to be completed in June 2021. 3 key findings →
Design: randomized controlled trial Evidence: high
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Stress granules (SGs) form during cellular stress and are implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). 4 key findings →
Evidence: low
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In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9). 3 key findings →
Design: cross-sectional Participants: 446 Evidence: low
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There is growing evidence that cognitive decline can be affected by both nutritional aspects and inflammation. 3 key findings →
Design: cross-sectional Participants: 116 Evidence: low
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In both its association with PD and its idiopathic form, RBD is an important risk factor for MCI. 2 key findings →
Evidence: low
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Rapid-eye-movement (REM) sleep behaviour disorder (RBD) is characterised by loss of muscular atonia and prominent motor behaviours during REM sleep. 2 key findings →
Evidence: low
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TDP-43 has been found in inclusion bodies of multiple neurological disorders, including amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease and Alzheimer's disease. 1 key finding →
Evidence: low
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Given that aging is associated with higher risk of cognitive decline and dementia, improving early detection of cognitive impairment has become a research and clinical priority. 4 key findings →
Participants: 200 Evidence: low
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All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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The new MRI rating scale for WMH in cholinergic pathways is reliable and shows stronger correlations with cognitive performance than a general WMH rating scale in AD with WMH. 3 key findings →
Participants: 60 Evidence: low
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This paper reviews current knowledge on sleep problems, sleep architecture changes and quantitative EEG alteration brought on by various neurodegenerative diseases, such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), REM sleep behavior disorder (RBD), Parkinson's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy MSA, Huntington's disease and Creutzfeldt-Jakob disease, in comparison to normal aging. 2 key findings →
Evidence: low
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Long sleep was associated with reduced overall cognitive function (β ± standard error = -0.25 ± 0.07, p < 0.001), with strongest effects in those with depressive symptoms using (-0.74 ± 0.30, p = 0.017) and not using antidepressants (-0.60 ± 0.26, p = 0.024). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →