Matrix metalloproteinases are versatile endopeptidases with many different functions in the body in health and disease. 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.
Matrix metalloproteinases are versatile endopeptidases with many different functions in the body in health and disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Central nervous system (CNS) immune privilege is an experimentally defined phenomenon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disruption of the tight junctions (TJs) of the blood-brain barrier (BBB) is a hallmark of many CNS pathologies, including stroke, HIV encephalitis, Alzheimer's disease, multiple sclerosis and bacterial meningitis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain perfusion is tightly coupled to neuronal activity, is commonly used to monitor normal or pathological brain function, and is a direct reflection of the interactions that occur between neuronal signals and blood vessels. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elimination of interstitial fluid and solutes plays a role in homeostasis in the brain, but the pathways are unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta-protein (Abeta) assembly into toxic oligomeric and fibrillar structures is a seminal event in Alzheimer's disease, therefore blocking this process could have significant therapeutic benefit. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain endothelial cells are unique among endothelial cells in that they express apical junctional complexes, including tight junctions, which quite resemble epithelial tight junctions both structurally and functionally. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reinvestigation of the chemical structure of beta-amyloid peptide (A beta) deposits in the vascular tissue of Alzheimer disease brains revealed that the 42-residue form A beta-(1-42), rather than the more soluble A beta-(1-40) form, is the predominant peptide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The molecular mechanism underlying the pathogenesis of the majority of cases of sporadic Alzheimer's disease (AD) is unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As a disease-modifying approach for Alzheimer's disease (AD), clioquinol (CQ) targets beta-amyloid (Abeta) reactions with synaptic Zn and Cu yet promotes metal uptake. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although biotherapeutics have vast potential for treating brain disorders, their use has been limited due to low exposure across the blood-brain barrier (BBB). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The A4 or beta-peptide (39 to 43 amino acid residues) is the principal proteinaceous component of amyloid deposits in Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes are perivascular cells with multifunctional activities which are now being elucidated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteins modified by advanced glycation endproducts (AGE) bind to cell surface receptors and other AGE binding proteins. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) is a major cause of vascular dementia and stroke. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dietary intake moderated the association between several cSVD biomarkers and MoCA scores such that the expected negative association between cSVD biomarkers and cognition was seen at low levels of healthy dietary intake, but not at medium or high levels. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified four SNPs (rs335929, rs335930, rs335931 and rs455671) were significantly associated with CSVD presence. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.0036), the MCRS group exhibited significantly worse performance on word list memory, word list recall, and MMSE-KC compared to the MCI group without slow gait. 2 key findings →
Participants: 81 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified 218 m6A sites significantly associated with the three diseases, highlighting 3,430 associations between m6A sites and gene expression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Exposure to fine particulate matter (PM ) pollution is associated with negative health outcomes including dementia, cardiovascular disease (CVD), and stroke due to increased levels of oxidative stress and inflammation among community-dwelling older adults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensity (WMH) is the core imaging hallmark of cerebral small vessel disease (CSVD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (CSVD) is a major contributor to stroke and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These dysregulations are associated with malfunctions in multiple signaling pathways or disrupted mechanical cellular responses. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
OCTA is a handy, noninvasive tool that enables the visualization of diminished retinal microvascular density in cases of early CSVD. 3 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Stroke is the leading cause of acquired disability. 2 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 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 →