27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The findings may help clinicians identify athletes who are at risk for worse impairments after a concussion due to preinjury sleep difficulties. 2 key findings →
Design: cohort study Participants: 348 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Sleep duration, psychiatric disorders and dementias are closely interconnected in older adults. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increasing evidence links cognitive-decline and Alzheimer's disease (AD) to various sleep disorders, including obstructive sleep apnea (OSA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
After multivariable adjustment, longer sleep duration was associated with lower Aβ42/40, poor sleep quality with higher NfL, daytime sleepiness with both lower Aβ42/40 and higher NfL, and insomnia symptoms with higher SPARE-AD. 3 key findings →
Participants: 1,325 Evidence: low
Full summary, score breakdown and related studies → Original source
Baseline pRBD was associated with faster decline in global cognition and all cognitive domains, including verbal episodic memory, visuospatial ability, executive function, language, and processing speed. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among community-dwelling older adults, reports of shorter sleep duration and poorer sleep quality are associated with greater Aβ burden. 4 key findings →
Design: cross-sectional Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Furthermore, PET studies have revealed that Aβ accumulates in the healthy brain after a single night of sleep deprivation, suggesting that the human glymphatic pathway might also be primarily active during sleep. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dysfunction in 24-h circadian rhythms is a common occurrence in ageing adults; however, circadian rhythm disruptions are more severe in people with age-related neurodegenerative diseases, including Alzheimer's disease and related dementias, and Parkinson's disease. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Prevalence of insomnia was 14%, 16%, and 11% for normal, MCI, and dementia groups. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The empirical study showed a U-shaped relationship between sleep duration and increased risk of cognitive impairment. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The final analytic sample included n = 2334 participants. 5 key findings →
Participants: 2,334 Evidence: low
Full summary, score breakdown and related studies → Original source
Methylation across all the CpGs strongly correlated with each other. 5 key findings →
Design: cross-sectional Participants: 96 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Around 40% of dementia risk is attributable to modifiable risk factors such as physical inactivity, hypertension, diabetes and obesity. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In IPTW, we observed a decreased risk of terminated healthspan for healthy sleep behaviors such as 'sleep duration 7-8h/d' (Hazard ratio, HR = 0.93; 95 % confidence interval, CI: 0.92-0.96; P < 0.001); 'morningness' (HR = 0.95; 95%CI: 0.93-0.98; P < 0.01); 'napping' (HR = 0.93; 95%CI: 0.91-0.94; P < 0.001); 'easy getting up from bed' (HR = 0.91; 95%CI: 0.88-0.93; P < 0.001); and, 'never/rarely experience sleeplessness/insomnia' (HR = 0.94; 95%CI: 0.92-0.96; P < 0.001). 5 key findings →
Participants: 590 Evidence: low
Full summary, score breakdown and related studies → Original source
Although some sleep disorders are markers of prodromal Parkinson's disease and dementia with Lewy bodies, it is unclear whether insomnia and somnolence can predict disease. 2 key findings →
Participants: 151 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Sample sizes for individuals with comorbid insomnia ranged from 23,168 (T2DM) to 3,015 (ADRDs). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Based on actigraphy as an objective measure of sleep time, melatonin is not an effective soporific agent in people with Alzheimer's disease. 3 key findings →
Participants: 157 Evidence: high
Full summary, score breakdown and related studies → Original source
Over 3.7 years, 22 patients phenoconverted (7 multiple system atrophy [MSA]; 15 Lewy body diseases [LBDs]). 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
long baseline nighttime and 24-h sleep durations (≥9 h) as well as being persistent or becoming long sleepers during follow-up were associated with dementia incidence. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher ISI score was associated with greater average levels of CSF Aβ42 (per point: 30.7 pg/mL, 95% CI: 4.17-57.3, p = 0.023), as was higher WASO (per 10 min: 136 pg/mL, 95% CI: 48-223, p = 0.002) and more awakenings (per 5:123 pg/mL, 95% CI = 55-192, p < 0.001). 4 key findings →
Design: cross-sectional Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source
Of the 17,668 respondents, 8,396 (47.5%) were men. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In participants with impaired cognition, baseline sleep apnea was related to better baseline MoCA performance (b = 0.65, 95% confidence interval [95% CI] = [0.07, 1.23]) and less decline in GCA over time (b = 0.06, 95% CI = [0.001, 0.12]). 5 key findings →
Participants: 5,822 Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The current review aims to examine melatonin therapy for both sleep disturbances and cognitive function in dementia. 2 key findings →
Participants: 520 Evidence: high
Full summary, score breakdown and related studies → Original source
Lower cerebrospinal fluid (CSF) ApoE, higher CSF p-tau181/amyloid-β (Aβ)42, and higher plasma p-tau231/Aβ42 were associated with higher variability of sleep midpoint, sleep duration, and/or activity count. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
9 of the 196 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
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 →