Aβ immunotherapy for Alzheimer's disease (AD) results in the removal of Aβ plaques and increased cerebral amyloid angiopathy (CAA). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Decades of research into anti-Aβ immunotherapies provide evidence for increased Aβ clearance from the brain; however, this is frequently accompanied by complicated vascular deficits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present data show that CAA plays a role in the development of microvascular lesions in the ageing brain, but cannot be considered as the most important factor in this vascular pathology, suggesting that other mechanisms also contribute importantly to the pathogenesis of microvascular changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The lymphatic clearance pathways of the brain are different compared to the other organs of the body and have been the subject of heated debates. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes are vascular mural cells embedded in the basement membrane of blood microvessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In cases of Alzheimer's presenile and senile dementia, Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT), respectively, we have observed, in addition to the gray matter degeneration, a lesion that has the character of an incomplete infarction confined to the white matter. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The cause of Alzheimer's disease (AD) is unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Blood-brain barrier (BBB), present at the level of the endothelium of cerebral blood vessels, selectively restricts the blood-to-brain paracellular diffusion of compounds; it is mandatory for cerebral homeostasis and proper neuronal function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurovascular dysfunction contributes to Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an age-related disorder characterized by progressive cognitive decline and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In all dementing illnesses, increased microvascular pathology was evident compared to normal controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular cognitive impairment is the second most common form of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because regional blood flow increases in association with the increased metabolic demand generated by localized increases in neural activity, functional imaging researchers often assume that changes in blood flow are an accurate read-out of changes in underlying neural activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transgenic mice that overexpress mutant human amyloid precursor protein (APP) exhibit one hallmark of Alzheimer's disease pathology, namely the extracellular deposition of amyloid plaques. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease directly implicated in Alzheimer's disease (AD) pathogenesis through amyloid-β (Aβ) deposition, which may cause the development and progression of dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The AT(N) research framework was introduced in 2018 to define Alzheimer's disease as a biological entity. 2 key findings →
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
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
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 amyloid angiopathy (CAA) is a cerebral small vessel disease caused by β -amyloid (Aβ) deposition at the leptomeningeal vessel walls. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA), one of the main types of cerebral small vessel disease, is a major cause of spontaneous intracerebral haemorrhage and an important contributor to cognitive decline in elderly patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is commonly found in older people and in patients with Alzheimer's disease (AD) accompanying cerebrovascular disorders and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes, as mural cells of microvessels, are important regulators of vascular structure formation and function maintenance in the process of cerebrovascular maturation, cerebrovascular homeostasis and disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
8 of the 228 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 8. The same 8 appear here every time.
- Haemodynamic impairment along the Alzheimer's disease continuum
- The blood-brain barrier in brain homeostasis and neurological diseases
- Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes
- Polygenic risk score predicts pathologically confirmed cerebral amyloid angiopathy
- The blood-brain barrier in health and chronic neurodegenerative disorders
- Blood-brain barrier opening in Alzheimer's disease using MR-guided focused ultrasound
- Three-dimensional brain-on-a-chip with an interstitial level of flow and its application as an in vitro model of Alzheimer's disease
- Greater White Matter Hyperintensity Volume Is Associated with the Number of Microhemorrhages in Preclinical Alzheimer's Disease
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
- Randomized / 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
- Multicenter 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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