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
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is characterized by cognitive dysfunction and progressive neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is recognized as multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The relationship between arterial hypertension and cognitive decline, two among the conditions with higher prevalence in the elderly population, has gained significant interest, in the scientific community, during the last few years, stemming from the numerous epidemiologic, experimental, and therapeutic evidences suggesting a non-casual correlation between the two conditions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Alzheimer's disease is characterized by aggregated amyloid beta plaques and neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metabolic syndrome (MetS) is an association between obesity, dyslipidemia, hyperglycemia, hypertension, and insulin resistance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large artery stiffness is a frequent condition that arises with ageing, and is accelerated by the presence of co-morbidities like hypertension, obesity and diabetes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Neurodegenerative disorders are the most devastating disorder of the nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Higher early-life CR (hazard ratio = 0.48, 95% CI = [0.21; 1.06]) but not early-life BR associated with a lower risk of incident dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Arterial hypertension is considered the main modifiable vascular risk factor that causes silent damage to brain vessels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
During the follow-up, we identified 159 incident dementia or CIND cases in total. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution is a multifaceted toxic chemical mixture capable of assaulting the central nervous system. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia has become a major public health concern around the world. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution is one of the greatest public health threats worldwide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological studies are associating elevated exposure to air pollution with increased risk of Alzheimer's disease and other neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
In these models, PM2.5 concentration was associated with smaller left hippocampal volume. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The third part of the DGP statement introduces the current body of knowledge on less studied health outcomes associated with exposure to ambient air pollution: the negative impact on metabolism leading to impaired glucose tolerance and diabetes as well as contribution to the development of neurodegenerative disorders and delayed cognitive function in children. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The ageing trajectory is plastic and can be slowed down by lifestyle factors, including good nutrition, adequate physical activity and avoidance of smoking. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
RECENT FINDINGS: Specific dietary patterns and varied nutrient combinations can have a protective effect on brain health, promote cognitive function, and mediate the comorbidity of chronic conditions associated with increased AD risk. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) incidence is increasing and with no disease modifying agents available, preventative measures through lifestyle factors are being investigated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Small vessel disease (SVD) refers to conditions where damage to arterioles and capillaries is predominant, leading to reduced, or interrupted perfusion of the affected organ. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (SVD) refers to a group of disease conditions affecting the cerebral small vessels, which include the small arteries, arterioles, capillaries, and postcapillary venules in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The median time interval between FSRP and death was 33.4 years for mid-life FSRP and 4.4 years for final FSRP measurement before death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perlecan is a heparan sulfate proteoglycan protein in the extracellular matrix that structurally and biochemically supports the cerebrovasculature by dynamically responding to changes in cerebral blood flow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,281 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 10. The same 10 appear here every time.
- Shared Causal Paths underlying Alzheimer's dementia and Type 2 Diabetes
- Hearing aid effectiveness and probable dementia risk across 33 countries: A pooled analysis of seven cohorts
- Crosstalk between Alzheimer's disease and diabetes: a focus on anti-diabetic drugs
- Ageing and Parkinson's disease: why is advancing age the biggest risk factor?
- Endothelial cells as key players in cerebral small vessel disease
- Regional differences in the incidence of Alzheimer’s disease and related dementias in South Carolina
- Risk of Dementia in Posttraumatic Stress Disorder
- Plasma tau, neurofilament light chain and amyloid-β levels and risk of dementia; a population-based cohort study
- Association of Leucocyte Telomere Length With Stroke, Dementia, and Late-Life Depression
- Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis
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 →