39/100
Cerebral small vessel disease (cSVD) is a major contributor to stroke, dementia, and cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral small vessel disease (CSVD) is one of the most common vascular diseases of the brain, primarily diagnosed using magnetic resonance imaging biomarkers. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
On March 12–14, 2024, the National Institute on Aging (NIA) together with the National Institute of Neurological Disorders and Stroke (NINDS) led a workshop exploring clinically meaningful changes in the context of Alzheimer's Disease and Alzheimer's Disease Related Dementias (AD/ADRD) clinical trials ( https://www.nia.nih.gov/research/dbsr/workshops/clinically‐meaningful‐outcomes‐ad‐adrd‐trials ). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In part 1 of the study, the patients with CSVD showed significant differences in Montreal Cognitive Assessment (MoCA), Auditory Verbal Learning Test (AVLT)-study, AVLT-immediate, AVLT-delay, AVLT-recognition, Trail Making Test (TMT)-A, TMT-B, and Verbal Fluency Test -fruits/vegetables compared with HCs. 5 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
During a median follow-up period of 4.6 years, stroke, MACEs, and AD dementia occurred in 24, 36, and 21 patients, respectively. 5 key findings →
Design: post-hoc analysis Participants: 1,011 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Elevated homocysteine in the blood, or hyperhomocysteinemia, is a recognized risk factor for multiple causes of dementia including Alzheimer’s disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The arteriosclerosis-dependent alteration of brain perfusion is one of the major determinants in small vessel disease, since small vessels have a pivotal role in the brain's autoregulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proper functioning of the brain is dependent on integrity of the cerebral vasculature. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A new study suggests that the leading genetic risk factor for Alzheimer's disease, apolipoprotein E4 (APOE4), is linked to blood-brain barrier breakdown and subsequent cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain capillary endothelial cells form the blood-brain barrier (BBB), which is covered with basement membranes and is also surrounded by pericytes and astrocyte end-feet in the neurovascular unit. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
RECENT FINDINGS: Many epidemiological studies have observed that circulating HDL levels associate with decreased Alzheimer's disease risk. 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
Insurmountable evidence has demonstrated a strong association between Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), along with various other cerebrovascular diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The median time interval between FSRP and death was 33.4 years for mid-life FSRP and 4.4 years for final FSRP measurement before death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While prevailing evidence supports that the amyloid cascade hypothesis is a key component of Alzheimer's disease (AD) pathology, many recent studies indicate that the vascular system is also a major contributor to disease progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent form of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes in the central nervous system attract growing attention of neurobiologists because of obvious opportunities to use them as target cells in numerous brain diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perlecan is a heparan sulfate proteoglycan protein in the extracellular matrix that structurally and biochemically supports the cerebrovasculature by dynamically responding to changes in cerebral blood flow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. 1 key finding →
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →