30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Structural and functional brain connectivity, synaptic activity, and information processing require highly coordinated signal transduction between different cell types within the neurovascular unit and intact blood-brain barrier (BBB) functions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diffusion in the extracellular space (ECS) of the brain is constrained by the volume fraction and the tortuosity and a modified diffusion equation represents the transport behavior of many molecules in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aging of the central nervous system and the development of incapacitating neurological diseases like Alzheimer's disease (AD) are generally associated with a wide range of histological and pathophysiological changes eventually leading to a compromised cognitive status. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It takes two to make blood vessels-endothelial cells and pericytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast to traditional neuroncentric views of Alzheimer's disease (AD), recent findings indicate that neurovascular dysfunction contributes to cognitive decline and neurodegeneration in AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
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
There has been a growing need for in vitro models of neurodegenerative diseases such as Alzheimer's disease that would enable a better understanding of etiology and faster development of treatment strategies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From a public health viewpoint, recognition of VCI before the development of dementia and correction of vascular burden on the brain may lead to a global decrease of incident dementia. 1 key finding →
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
Cerebrospinal fluid (CSF) circulation and turnover provides a sink for the elimination of solutes from the brain interstitium, serving an important homeostatic role for the function of the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alterations in cerebrovascular regulation related to vascular oxidative stress have been implicated in the mechanisms of Alzheimer's disease (AD), but their role in the amyloid deposition and cognitive impairment associated with AD remains unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease. 1 key finding →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flows through perivascular spaces (PVSs) surrounding brain vasculature, and impaired flow has been linked to neurodegenerative diseases such as Alzheimer’s. However, the mechanisms driving CSF flow and its oscillatory dynamics remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence and expert opinion suggest that subcortical microhaemorrhages may be less closely related to cerebral amyloidosis than lobar lesions and may therefore warrant separate consideration in anti-amyloid treatment eligibility criteria. 5 key findings →
Design: longitudinal study Participants: 1,146 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is accompanied by profound cerebrovascular dysfunction, yet it remains unclear whether endothelial abnormalities reflect only vascular injury or altered regulatory states connecting vascular remodeling with metabolic and immune function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular pathology is an important contributor to dementia, and astrocyte dysfunction is increasingly recognized as a key mediator of cerebrovascular injury. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A major obstacle to effective Alzheimer’s disease therapy is the limited ability to deliver therapeutics across the blood-brain barrier. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-Aβ immunotherapies for Alzheimer’s Disease (AD) have high rates of amyloid-related imaging abnormalities (ARIA), an adverse side effect with markedly higher rates in APOE4 carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 233 studies in this tag that have a study page, 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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events