Alzheimer's disease (AD) is a neurodegenerative disorder associated with the progressive dysfunction of cognitive ability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a neurodegenerative disorder associated with the progressive dysfunction of cognitive ability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A linear mixed effects model revealed a significant interaction in the right parietal lobe: the MCI group showed increased connectivity while the healthy elders showed decreased connectivity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The retina offers a unique "window" to study pathophysiological processes of dementia in the brain, as it is an extension of the central nervous system (CNS) and shares prominent similarities with the brain in terms of embryological origin, anatomical features and physiological properties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In diabetic retinopathy, venous oxygen saturation increases and arteriovenous difference decreases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent failure of several clinical trials on anti-β-amyloid (Aβ) drugs in Alzheimer's disease (AD) suggested earlier intervention in the disease course. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurological disorder having two major pathological hallmarks: the extracellular senile plaques and intracellular neurofibrillary tangles composed of amyloid beta protein and hyperphosphorylated tau respectively. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease progressively impairs cognition and daily function, and death usually occurs five to ten years after diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast to the idea that tau phosphorylation is toxic, Ittner et al. (2016) recently showed that specific tau phosphorylation is neuroprotective, phenocopying tau ablation (DeVos et al., 2017), thus highlighting the complex tau biology that underlies neurotoxicity and neuroprotection. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
With an ageing global population, the number of people with dementia, and its main cause Alzheimer's disease (AD), is growing. current licensed treatments available for ad are only alleviate the symptoms of the disease, and are effective only in some people with ad for a limited time. there are currently no therapies that target the disease process. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques enriched with extracellular amyloid beta (Aβ) and intracellular neurofibrillary tangles comprised of hyperphosphorylated tau proteins are the two main pathological hallmarks of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of Alzheimer's disease (AD) continues to rise, while treatment options for cognitive impairment are limited. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this report we assessed by docking and molecular dynamics the binding mechanisms of three FDA-approved Alzheimer drugs, inhibitors of the enzyme acetylcholinesterase (AChE): donepezil, galantamine and rivastigmine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The major pharmacokinetic interactions identified concerned fluoxetine, paroxetine and ketoconazole when used with galantamine or donepezil. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular cognitive impairment (VCI) is the second most common type of dementia after Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The objective of the review is to assess the effect of metformin on the risk, progression and severity of Alzheimer's disease and other forms of dementia, as well as any measures of cognitive performance or impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results of epidemiological and pathophysiological studies suggest that type 2 diabetes mellitus (T2DM) may predispose to Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As patients lose cognitive function, they lose autonomy and increasingly use fiscal, social, and medical resources. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The incidence of dementia is expected to double in the next 20 years and will contribute to heavy social and economic burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A significant body of evidence supports the protective role of exercise training (ET) in cardiovascular diseases, skeletal muscle dystrophies, several types of cancer, Alzheimer disease or even in the recovery of spinal cord injury. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increased age is associated with normative declines in both sleep and cognitive functioning. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The endogenous circadian rhythms are one of the cardinal processes that control sleep. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a significant public health concern. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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 →