Microglial activation participates in white matter injury after cerebral hypoperfusion. 4 key findings →
Participants: 80 Evidence: low
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29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Microglial activation participates in white matter injury after cerebral hypoperfusion. 4 key findings →
Participants: 80 Evidence: low
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In linear mixed models, vascular endothelial growth factor was significantly associated with incident DWI-positive lesions over 1 year. 5 key findings →
Design: cross-sectional Participants: 181 Evidence: moderate
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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
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Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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A total of 261 patients (75.3±6.8 years) were recruited from a memory-clinic cohort. 5 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 29 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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This human study is based on an established cohort of "SuperAgers," 80+-year-old individuals with episodic memory function at a level equal to, or better than, individuals 20-30 years younger. 4 key findings →
Participants: 21 Evidence: moderate
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The presence of either severe WMH or MTA was associated with a modest but non-significant increase in frequency of mild cognitive deficits (severe WMH: odds ratio (OR) = 1.9 (95% confidence interval (CI), 1.0 to 3.7); MTA present: OR = 1.5 (95% CI, 0.8 to 2.8)). 2 key findings →
Participants: 639 Evidence: low
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The prevalence of ICAS in older adults is high, and it could be a target for primary prevention of stroke and dementia in this population. 3 key findings →
Participants: 1,765 Evidence: moderate
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Wakefulness, along with fast cortical rhythms and associated cognition, depend on the basal forebrain (BF). 3 key findings →
Evidence: low
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Accumulation of mononuclear phagocytes [monocytes, macrophages, and dendritic cells (DCs)] in the vessel wall is a hallmark of atherosclerosis. 4 key findings →
Evidence: low
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This is the first study to assess cerebral microinfarcts (CMIs) on 3 tesla (3T) magnetic resonance imaging (MRI) in a memory clinic population. 4 key findings →
Participants: 238 Evidence: low
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We included 88 patients with dementia due to AD from the Amsterdam Dementia Cohort. 4 key findings →
Participants: 88 Evidence: moderate
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On long-term follow-up (median 15 years; minimum-maximum, 0-20), participants developed cardiometabolic disease (hypertension [1255 events]; diabetes [381 events]), chronic kidney disease (529 events), dementia (235 events), cardiovascular disease (684 events) a 4 key findings →
Evidence: low
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New hippocampal neurons are continuously generated in the adult brain. 4 key findings →
Evidence: low
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= 0.008). Deficits in medial temporal CVR are observed in older adults with MCI and are related to worse memory function. 4 key findings →
Design: cross-sectional Evidence: moderate
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In total, 156 individuals were assessed for eligibility, and 79 (51%) were recruited (mean age 61.6 ± 6.9 (range 60-75) years; 68% male). 5 key findings →
Participants: 156 Evidence: high
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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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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →
Participants: 40,000 Evidence: low
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Our aim is to examine the interplay between cerebral small vessel disease (CSVD) pathology, Alzheimer’s disease (AD) related amyloid-β (Aβ) clearance, and cognition in general population. 2 key findings →
Design: cross-sectional Participants: 1,026 Evidence: moderate
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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
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Our data suggest that vascular abnormalities, independently of blood pressure levels, may play a role in the setting of subjective memory complaints as well as of WMH in elderly hypertensive patients. 4 key findings →
Design: cross-sectional Evidence: low
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The results underscore the importance of reducing the number of cardiovascular risk factors for maintaining CBF and cognition in an aging population. 5 key findings →
Participants: 69 Evidence: low
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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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% 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 →