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
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
The primary outcome of this clinical trial is the change in the Vascular Dementia Assessment Scale-cognitive subscale from baseline to 12 months. 3 key findings →
Participants: 1,052 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The glymphatic system, a vital brain perivascular network for waste clearance, hinges on the functionality of the aquaporin 4 (AQP4) water channel. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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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Among 1154 participants (46% men, mean age 70.9±8.7 years), 92 (8%) developed stroke over a median follow-up of 8.6 years (Q1-Q3: 5.1-12.5). 5 key findings →
Participants: 1,154 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
=0.002). Early-onset CHD and genetic susceptibility are associated with a higher risk of incident dementia and a larger WMH volume. 2 key findings →
Design: cohort study Participants: 671 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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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The mean age of the participants was 68 ± 9 years and 39% were female. 5 key findings →
Design: post-hoc analysis Participants: 759 Evidence: low
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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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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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= 0.026). Complementing previous research that focuses on CSVD and white matter changes, our study highlights abnormal gray matter integrity as a possible link between small vessel pathology and cognitive disorders. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
• 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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They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia. 5 key findings →
Participants: 1,072 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 total of 197 participants were included in the study. 5 key findings →
Participants: 197 Evidence: low
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WMH burden positively correlated to Neurofilament-Light (NfL) and pTau181. 5 key findings →
Design: cross-sectional Participants: 583 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The final analysis included 459,924 participants. 5 key findings →
Participants: 459,924 Evidence: moderate
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hexanucleotide repeat expansions (HRE) and WMH in bvFTD patients. bvFTD and svPPA are associated with elevated WMH burden independent of CVRF. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MCI exhibited greater retinal tortuosity (p < 0.05) and sparser vasculature (p < 0.001), correlating with higher PSMD, WMH volumes, and adverse plasma biomarkers (all p < 0.05). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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.
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