Multifactorial mechanisms underlying late-onset Alzheimer's disease (LOAD) are poorly characterized from an integrative perspective. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our study establishes a connection between Aβ antibodies engaged at CAA deposits, the activation of perivascular macrophages, and the upregulation of genes involved in vascular permeability. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data suggest that vascular leakage events, such as microhemorrhage, may be related to the removal of vascular Aβ. 5 key findings →
Participants: 345 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Cerebral blood flow is reduced early in the onset of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results of this study showed global BBB leakage in patients with early AD that is associated with cognitive decline. 4 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
High-speed high-resolution imaging of the whole-brain hemodynamics is critically important to facilitating neurovascular research. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perivascular spaces (PVS) are compartments surrounding cerebral blood vessels that become visible on MRI when enlarged. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-associated cerebral small vessel disease (CSVD) represents a clinically heterogenous condition, arising from diverse microvascular mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques, consisting of deposited beta-amyloid (Aβ), are a neuropathological hallmark of Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ischemic stroke and vascular cognitive impairment, caused by a sudden arterial occlusion or more subtle but protracted vascular insufficiency, respectively, are leading causes of morbidity and mortality worldwide with limited therapeutic options. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA) are parenchymal edema/effusion and hemorrhage that occur as side effects of immunotherapies targeting beta-amyloid for patients with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the accumulation of amyloid-beta (Aβ) in the walls of cerebral vessels. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) is a critical structure for maintaining homeostasis in the central nervous system, and its dysfunction is widely implicated in the pathogenesis and progression of various neurological disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Worldwide, around 50 million people live with dementia, and this number is projected to triple by 2050. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (SVD) is a vascular disorder that increases the risk of stroke and dementia and is diagnosed through brain MRI. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With our focus on Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), the authors herein provided a comprehensive overview of impaired amyloid beta and tau clearance pathways observed through advanced neuroimaging techniques such as dynamic contrast-enhanced MR imaging, arterial spin labeling, phase contrast MR imaging, PET, and functional MR imaging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVDs) account for 25% of stroke and are a frequent cause of cognitive or motor disability in adults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) is the most common cause of vascular cognitive impairment and dementia (VCID) and highly associated with Alzheimer's disease pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease is a neurological disease that affects the brain microvasculature and which is commonly observed among the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Arteriole medin was higher in those with AD, VaD, or combined AD/VaD versus ND (P < .05), and correlated with tangle, plaque, and WML, but not CAA or CoW atherosclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic neuroinflammation is a principal cause of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease and glymphatic dysfunction are anatomically connected and significant risk factors are shared between the two. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic cerebral amyloid angiopathy is a common, well-defined small vessel disease and a largely untreatable cause of intracerebral haemorrhage and contributor to age-related cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
9 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 9. The same 9 appear here every time.
- The blood-brain barrier in brain homeostasis and neurological diseases
- Hemostasis components in cerebral amyloid angiopathy and Alzheimer's disease
- ADAMTS13 maintains cerebrovascular integrity to ameliorate Alzheimer-like pathology
- Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression
- The blood-brain barrier in Alzheimer's disease
- Association of Cardiovascular Risk Factors with Cerebral Perfusion in Whites and African Americans
- Vascular cognitive impairment - Past, present, and future challenges
- Vasomotion as a Driving Force for Paravascular Clearance in the Awake Mouse Brain
- Magnetic Resonance Imaging of Blood-Brain Barrier permeability in Dementia
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 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.
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 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