The small effect of VRFs and LAD on WMH suggests that WMH have a large "nonvascular," nonatheromatous etiology. 3 key findings →
Participants: 881 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
55/100
Cerebrovascular reactivity (CVR) deficits may contribute to small vessel disease, such as white matter hyperintensities (WMH). 2 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source
SES and LA were associated with better cognitive performance at baseline, but were not associated with cognitive decline over time. 5 key findings →
Design: longitudinal study Participants: 181 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The etiology of cerebrovascular pathology is heterogeneous. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93). 5 key findings →
Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Twenty-four patients of comparable age, blood pressure, and degree of dementia were classified by an "Ischemic Score" based on clinical features into "multi-infarct" and "primary degenerative" dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Accumulating evidence implicates small vessel cerebrovascular disease, visualized as white matter hyperintensities (WMH) on T2-weighted magnetic resonance imaging, in the pathogenesis and diagnosis of Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Diabetes was not associated with brain atrophy cross-sectionally or longitudinally. 5 key findings →
Design: cross-sectional Participants: 112 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study included 3540 participants with RVC data and 489 with WMH data (median [IQR] age: 73.2 [71.4-76.3] and 72.5 [71.2-75.4] years; female: 52.9% and 47.6%) over a median follow-up of 7.4 [IQR 5.5-8.5] and 3.8 [IQR 2.9-5.3] years, respectively. 5 key findings →
Design: cross-sectional Participants: 3,540 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cognitive deficits in VaD and VCI are characterized by disturbance of frontal functions, with less verbal memory impairment. 2 key findings →
Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that genes associated with clinical neurological disease also have detectable effects on subclinical phenotypes. 5 key findings →
Participants: 705 Evidence: low
Full summary, score breakdown and related studies → Original source
These cross-sectional results suggest that cortical changes (regional-specific damage and network breakdown), mediated (in)directly by WMH (tract-specific damage) and other factors (eg, vascular risk factors), might lead to cognitive decline. 5 key findings →
Design: cross-sectional Participants: 426 Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensity (WMH), indicative of cerebral small vessel disease, has emerged as a potential biomarker for cognitive decline in Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 158 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Five WMH clusters emerged. Compared to those with low WMH burden, participants in the mild occipital and high parieto-occipital clusters had faster memory decline; mild fronto-parietal and high parieto-occipital clusters showed faster executive decline; and mild and high fronto-parietal and high parieto-occipital clusters had faster language decline. 5 key findings →
Design: longitudinal study Participants: 1,047 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Type 2 diabetes mellitus (T2DM) and major depressive disorder (MDD) are reciprocal risk factors, and both elevate dementia risk. 4 key findings →
Participants: 15,765 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.025) over 3 years. NfL was not significantly associated with any MRI cSVD marker. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
50/100
The results suggest that the hippocampus and the temporal horn of the lateral ventricles may be useful as antemortem markers of AD in mildly impaired patients. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundThe progression of cerebral small vessel disease (CSVD) leads to cognitive decline, which can be categorized into subcortical vascular mild cognitive impairment (svMCI) and vascular dementia (VaD).ObjectiveThis research aimed to examine the structural changes in gray (GM) and white matter (WM) in the brain across the disease spectrum. 5 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
MAFLD was associated with an increased risk of WMH over 4.1 years in middle‐aged adults. 5 key findings →
Participants: 2,155 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results pertaining to menopause-related characteristics, such as age at menopause or menopause hormonal therapy, did not replicate the literature reporting an association with WMH volumes. 5 key findings →
Design: cross-sectional Participants: 9,560 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (cSVD) is characterised by white matter hyperintensities (WMH) and contributes to stroke and dementia. 5 key findings →
Design: cross-sectional Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities (WMH) are neuroimaging markers linked to an elevated risk of cognitive decline. 2 key findings →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 225 patients (mean age 65.4 years, 54.2% male), MCR prevalence was 16.4%. 5 key findings →
Design: cross-sectional Participants: 225 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Diabetic patients are at increased risk for stroke, but little is known about the presence of other brain lesions. 3 key findings →
Participants: 1,252 Evidence: low
Full summary, score breakdown and related studies → Original source
We included 110 patients with CAA (strictly lobar ICHs/CMBs), 33 with HA (strictly deep ICHs/CMBs) and 97 with mixed lobar/deep ICHs/CMBs. 5 key findings →
Participants: 110 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →