32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Greater arterial stiffness and pressure pulsatility are associated with brain aging, MRI vascular insults, and memory deficits typically seen in Alzheimer dementia. 2 key findings →
Participants: 1,587 Evidence: low
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The association between moderate-severe chronic kidney disease and white matter hyperintensity volume highlights the growing importance of kidney disease as a possible determinant of cerebrovascular disease and/or as a marker of microangiopathy. 5 key findings →
Participants: 615 Evidence: moderate
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These cross-sectional data provide evidence that tHcy is a risk factor for white matter damage. 1 key finding →
Design: cross-sectional Participants: 259 Evidence: low
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In a previous study of normal elderly male twins, the heritability of quantitative white matter hyperintensity (WMH) volume has been estimated to be high (0.73). 4 key findings →
Participants: 2,012 Evidence: moderate
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Although observational data cannot establish causality, our findings are consistent with the hypothesis that decreasing cardiac function, even at normal cardiac index levels, is associated with accelerated brain aging. 5 key findings →
Evidence: moderate
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Stepwise decreases in WM integrity as measured by both DTI and FLAIR were independently associated with stepwise increases in WMH risk, emphasizing that these modalities may provide complementary information for understanding the time course of aging-associated WM degeneration. 3 key findings →
Design: longitudinal study Evidence: moderate
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Among 2935 patients (50.4% women; mean age=72.2 years; 19.8% subjective cognitive impairment, 39.8% mild cognitive impairment, and 40.4% dementia), larger WMH volume within projection fibres (B=0.24, SE=0.10, p=0.013) was associated with greater apathy. 5 key findings →
Participants: 2,935 Evidence: low
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55 of the 152 (36.2 %) aMCI subjects progressed to AD. 3 key findings →
Evidence: low
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Amnestic forms of MCI appear to have demographic, genetic, and MRI findings suggestive of Alzheimer disease pathology, whereas the nonamnestic forms of MCI have findings suggestive of vascular disease. 4 key findings →
Design: cross-sectional Participants: 153 Evidence: low
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FSRP and several cardiovascular risk factors were related to both WMHV measured continuously and to a categorical designation of large volumes of WMH. 3 key findings →
Evidence: moderate
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A significant ADI × dementia interaction was observed for global atrophy (p = .005) and several other outcomes. 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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Aβ and vascular risk interact to enhance cortical thinning in posterior brain regions that are particularly vulnerable to AD. 3 key findings →
Evidence: low
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The duration and lifetime pattern of hypertension is related to risk of stroke and dementia. 4 key findings →
Participants: 1,686 Evidence: moderate
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We determined the relationship between apolipoprotein (Apo)E, MRI, and low cognitive scores. 1 key finding →
Evidence: low
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Midlife hearing loss was associated with smaller brain volumes, accelerated decline in executive function, accelerated accrual of white matter abnormalities, and a near doubling of dementia risk, suggesting a potential causal or biomarker role for midlife hearing loss in the prevention of late‐life dementia. 4 key findings →
Participants: 1,656 Evidence: low
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In 3413 participants (mean age: 59 ± 14 years, 53.4% women), 11% had prevalent CVD or AF, 8% had prevalent CVD, and 4% had prevalent AF. 5 key findings →
Participants: 3,413 Evidence: moderate
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Cognitively normal subjects with HTN (n=19) had decreased rCBF in the putamen, globus pallidus, bilaterally, and in the left hippocampus compared with normotensives (n=22). 1 key finding →
Participants: 19 Evidence: low
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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
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We found that ∼25% of donors lived in high deprivation contexts, 52% had at least one incidence of CVD, and the cohort identified as .05). 3 key findings →
Participants: 7,187 Evidence: moderate
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We found differential region-specific associations between degenerative and vascular processes and the structural integrity of the CC across the spectrum of cognitive ability. 5 key findings →
Evidence: low
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Higher teacher‐student ratio was associated with greater gray matter volume (β = 6.25, 95% CI: 1.57, 10.92) but was not associated hippocampal volume (β = ‐0.01, 95% CI: ‐0.14, 0.11), ventricular volume (β = ‐0.04, 95% CI: ‐0.13, 0.04), or white matter hyperintensity (β = ‐0.02, 95% CI: ‐0.31, 0.26) (Table 2). 5 key findings →
Participants: 450 Evidence: moderate
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Mineralized blood vessels (MBV) are a form of vascular pathology associated with cerebrovascular aging and neurodegeneration; however, their regional distribution and clinicopathological correlates in Alzheimer disease (AD) remain poorly characterized. 4 key findings →
Evidence: low
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With elevated HbA1c, greater LA-derived diol/epoxide ratios were associated with greater WMH volume (β [95% CI] = 0.565 [0.100, 1.030], p = 0.017), lower global BPF (β [95% CI] = -0.476 [-0.903, -0.048], p = 0.029), and poorer memory performance (β [95% CI] = -0.603 [-1.070, -0.136], p = 0.012), such that detrimental associations were observed only in T2DM. 5 key findings →
Evidence: low
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Dietary intake moderated the association between several cSVD biomarkers and MoCA scores such that the expected negative association between cSVD biomarkers and cognition was seen at low levels of healthy dietary intake, but not at medium or high levels. 3 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. 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 32,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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
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