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
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
The ALPS-index showed a stepwise decline with increasing WMH severity and cognitive impairment (p < 0.001). 5 key findings →
Participants: 124 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• Anterior cingulate cortex (ACC) hypometabolism is a non-specific finding in many brain disorders. • ACC hypometabolism was more common in vascular cognitive impairment and dementia (VCID) than Alzheimer dementia (AD). • ACC hypometabolism correlated with cerebral small vessel disease markers. • ACC hypometabolism may be associated with motor stereotypies in VCID. • FDG-PET patterns of hypometabolism may identify vascular contributions to cognitive impairment The anterior cingulate cortex (ACC) is an important hub in the executive and salience networks. 2 key findings →
Participants: 379 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma Aβ levels and regional WMH burden are associated with glymphatic dysfunction as indicated by reduced ALPS. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (CSVD) is composed of several diseases affecting the small arteries, arterioles, venules, and capillaries of the brain, and refers to several pathological processes and etiologies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diffusion-tensor imaging (DTI) is a noninvasive medical imaging tool used to investigate the structure of white matter. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) is a major cause of stroke and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The cerebral vascular system stringently regulates cerebral blood flow (CBF). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular cognitive impairment (VCI) is a major health challenge and represents the second most common cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alterations in cerebral blood flow are common in several neurological diseases among the elderly including stroke, cerebral small vessel disease, vascular dementia, and Alzheimer's disease. 4D flow magnetic resonance imaging (MRI) is a relatively new technique to investigate cerebrovascular disease, and makes it possible to obtain time-resolved blood flow measurements of the entire cerebral arterial venous vasculature and can be used to derive a repertoire of hemodynamic biomarkers indicative of cerebrovascular health. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mechanism whereby an increase in neuronal activity (NA) leads to a local elevation in cerebral blood flow to supply the active neurons with oxygen and nutrients and remove the catabolic waste has been termed neurovascular coupling (NVC). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and cerebral small vessel disease (cSVD) are the two main causes of dementia with blood-brain barrier (BBB) breakdown being a common contributor. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMHs) and cerebral β-amyloid (Aβ) have been characterized as clinically significant biomarkers associated with greater cognitive decline and incidence of Alzheimer's Disease (AD) dementia. 3 key findings →
Participants: 523 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patient inclusion started in January 2023, and study enrollment of patients is expected to finish in the second quarter of 2027, whereas the main results are expected to be published in the first quarter of 2028. 5 key findings →
Design: cross-sectional Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using a unique dataset of the same participants scanned close in time on different scanner and protocols, we found that (1) MMD measurements were useful to test the need/improvement due to harmonization; (2) ComBat was not substantially better at creating compatible distributions between scanner vendors than Deming regression, and both were sometimes inadequate. 4 key findings →
Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
40/100
These data suggest that low-grade inflammation as assessed by high-sensitivity C-reactive protein is associated with cerebral microstructural disintegration that predominantly affects frontal pathways and corresponding executive function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (CSVD) is the most common, chronic and progressive vascular disease. 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
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
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
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
Sex differences exist in how cerebral blood vessels function under both physiological and pathological conditions, contributing to observed sex differences in risk and outcomes of cerebrovascular diseases (CBVDs), such as vascular contributions to cognitive impairment and dementia (VCID) and stroke. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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