Alzheimer's disease (AD) is a significant public health concern. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The nerve center responsible for controlling our circadian rhythm is located in a cluster of cells known as the suprachiasmatic nucleus in the hypothalamus. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Serious OSAS and short sleep duration are associated with a high risk of developing dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Obstructive sleep apnea (OSA) is a prevalent sleep related breathing disorder characterized by repetitive collapse of the upper airways leading to intermittent hypoxia and sleep disruption. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is increasing in prevalence and has a significant impact on caregivers and the healthcare system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disturbances such as insomnia, hypersomnia, and circadian rhythm disturbance are common in normal elderly and Alzheimer's disease (AD) patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The article reviews the phenomenology of sleep and wakefulness disorders in Parkinson's disease and Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), which accounts for most of the dementia cases, is, aside from cognitive deterioration, often characterized by the presence of non-cognitive symptoms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia and currently there are no effective disease-modifying treatments available. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
In the world, the spread of hearing loss due to age is an important socio-medical problem. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Many studies have focused on the relationship between hearing loss and Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Presbycusis, or age-related hearing loss (ARHL), is the result of physiologic and pathologic changes associated with advancing age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In addition to the well-documented relationship between peripheral hearing loss and cognition highlighted in previous comprehensive reviews, there is also some evidence to suggest that there is a relationship between central hearing impairment and cognition. 4 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related hearing loss is a multifactorial condition that affects more than one-third of the aging population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hearing loss has been recently ranked as the fifth leading cause of years lived with disability, ahead of many other chronic diseases such as diabetes, dementia, or chronic obstructive pulmonary disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A multitude of different neurocognitive screening tests and detailed test batteries are available, particularly in the field of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hearing loss can be caused by a number of different pathological conditions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Studies have linked obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD) and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) often coexists with other aging-associated diseases including obesity, diabetes, hypertension, and cardiovascular diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this review, we will discuss the possible mechanisms which may relate the association between MetS and cognitive decline which include vascular damages, elevation of reactive oxygen species (ROS), insulin resistance and low-grade inflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metabolic syndrome (MetS) is a common and complex disorder combining hypertension, obesity, dyslipidemia, and insulin resistance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Innumerable studies have suggested "the lower, the better" for cardiovascular risk factors, such as body weight, lipid profile, blood pressure, and blood glucose, in terms of health outcomes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Diabetes, obesity, and Alzheimer's disease (AD) are associated with vascular complications and impaired nitric oxide (NO) production. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Until recently, intraindividual visit-to-visit variability of cardiovascular risk factors has been dismissed as random fluctuation. 1 key finding →
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 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.
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 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 →