30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
This raises the suggestion that a decreased neurovascular coupling in the disease process of AD is related to comorbid small vessel disease. 2 key findings →
Participants: 119 Evidence: moderate
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Cerebral small vessel disease (cSVD) is associated with vascular cognitive impairment, dementia, and stroke. 3 key findings →
Design: cross-sectional Participants: 59 Evidence: low
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Hyperhomocysteinemia (HHcy) is an established risk factor for cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 507 Evidence: moderate
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Alzheimer's disease (AD) and vascular dementia (VaD) exhibit distinct neuropathological hallmarks, with AD defined by cortical amyloid plaques and neurofibrillary tangles, while VaD arises primarily from cerebrovascular disease (CeVD). 4 key findings →
Participants: 531 Evidence: moderate
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Temporoparietal hypoperfusion on SPECT is common to both AD and DLB. 2 key findings →
Participants: 23 Evidence: low
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Our results suggest that different subcortical areas have different vulnerabilities to ischemia in CADASIL. 4 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
Among participants with normal cognition, higher aortic PWV related to lower frontal lobe CBF (β=-0.43; P=0.04) and higher CVR in the whole brain (β=0.11; P=0.02), frontal lobes (β=0.12; P<0.05), temporal lobes (β=0.11; P=0.02), and occipital lobes (β=0.14; P=0.01). 3 key findings →
Participants: 155 Evidence: low
Full summary, score breakdown and related studies → Original source
Pulse pressure, but not mean arterial pressure, significantly mediated the relationship between age and white matter hyperintensity load. 5 key findings →
Design: cohort study Evidence: moderate
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The plasma PlGF level was significantly elevated in patients with SIVD compared with CUCs, and showed a high accuracy with an area under the curve of 0.893. 5 key findings →
Participants: 102 Evidence: moderate
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• Patients with Parkinson's disease (PD) and cognitive impairment demonstrated a significantly greater burden of white matter hyperintensities (WMH), with the highest burden observed in those with PD dementia. 5 key findings →
Participants: 122 Evidence: low
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WMH shape is associated with long-term risk for dementia after 10 years in community-dwelling older adults. 2 key findings →
Participants: 2,493 Evidence: low
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< 0.1). -ε4 status, and Aβ load, and not mediated by markers of neuroaxonal degradation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities (WMH) are associated with cortical thinning in distant brain regions. 5 key findings →
Design: cross-sectional Participants: 551 Evidence: moderate
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Individuals with msWMH showed systematic deficits in face-memory processing across encoding, maintenance, and retrieval, accompanied by reduced theta power and synchronization, altered alpha power, and disrupted theta-gamma coupling. 5 key findings →
Design: longitudinal study Evidence: moderate
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A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 197 participants were included in the study. 5 key findings →
Participants: 197 Evidence: low
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Genetic variants increase the risk of neurocognitive disorders in later life, including vascular dementia (VaD) and Alzheimer’s disease (AD), but the precise relationships between genetic risk factors and underlying disease etiologies are not well understood. 4 key findings →
Evidence: low
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Amyloid status moderated associations between IIV-dispersion and WMH, such that higher IIV-dispersion was associated with greater WMH in Aß+ individuals whether WMH was examined as a continuous (B = 0.30, ß = 0.13, p = .006) or a dichotomous variable based on quartiles (odds ratio [OR] = 2.41, p < .001). 4 key findings →
Participants: 819 Evidence: low
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= 0.71) longitudinally. YKL-40 associations with FW and FW-corrected fractional anisotropy were null. 4 key findings →
Design: cross-sectional Evidence: moderate
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Each 1-SD increase in eGDR was significantly associated with a reduction in WMH volume (β = -0.057; 95% CI: -0.062 to -0.051; p 0.05). 3 key findings →
Participants: 34,789 Evidence: moderate
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Lower DTI-ALPS, lower BOLD-CSF coupling, and higher CP volume predicted dementia, but PVS volume did not. 5 key findings →
Evidence: low
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Diffusion tensor measurements correlate better with cognition than conventional MRI measures. 3 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
3D-SSP enables quantitative data extraction and reliable localization of metabolic abnormalities by means of stereotactic coordinates. 2 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
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.
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.
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