27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among 11 601 participants (mean [SD] age, 59.18 [9.41] years; 5569 male [48.0%]), 9145 (78.8%) were exposed to at least 1 ACE indicator, 4241 (36.6%) to at least 1 AAE indicator, and 3531 (30.4%) to both ACE and AAE markers. 5 key findings →
Design: cohort study Participants: 601 Evidence: moderate
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A total of 42 342 participants from the pooled cohorts were included (mean [SD] age, 61.3 [9.8] years; 55.0% female). 5 key findings →
Design: cohort study Participants: 342 Evidence: moderate
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The telmisartan group had the lowest risk of all dementias (telmisartan vs NT-ARB: hazard ratio [HR]: 0.78; 95% confidence interval [CI]: 0.60 to 1.01; telmisartan vs angiotensin-converting enzyme inhibitor: HR: 0.67; 95% CI: 0.48 to 0.94). 5 key findings →
Design: cohort study Participants: 39,665 Evidence: moderate
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Multiple MTHFR coding variants were identified in this small Indonesian VaD cohort. 2 key findings →
Design: cross-sectional Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMHs) are neuroimaging markers widely interpreted as caused by cerebral small vessel disease, yet emerging evidence suggests that a subset may have a neurodegenerative etiology. 1 key finding →
Participants: 32,526 Evidence: moderate
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People with severe mental illnesses (SMIs), including schizophrenia spectrum disorders (SSD), major depressive disorder (MDD), and bipolar disorder (BD), experience elevated rates of physical comorbidity and premature mortality. 3 key findings →
Design: cross-sectional Participants: 694,086 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →
Design: longitudinal study Participants: 494 Evidence: moderate
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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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Considerable data support the presence of both systemic and CNS inflammation in SVD and VCID. 3 key findings →
Design: longitudinal study Evidence: moderate
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= 0.028), but not with progression of BG-EPVS or WMHs at follow-up. 5 key findings →
Design: cohort study Evidence: moderate
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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
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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
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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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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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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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Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD). 2 key findings →
Evidence: low
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The brain endothelial Gαq/11 signalling pathway preserves normal vascular reactivity, and its loss resembles mild endothelial dysfunction in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mercury remains a pervasive environmental neurotoxicant strongly implicated in hippocampal oxidative injury and dementia-related cognitive decline, yet safe multi-target agents against its neurotoxicity remain limited. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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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
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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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Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →
Evidence: low
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Plasma Aβ levels and regional WMH burden are associated with glymphatic dysfunction as indicated by reduced ALPS. 3 key findings →
Participants: 216 Evidence: low
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In part 1 of the study, the patients with CSVD showed significant differences in Montreal Cognitive Assessment (MoCA), Auditory Verbal Learning Test (AVLT)-study, AVLT-immediate, AVLT-delay, AVLT-recognition, Trail Making Test (TMT)-A, TMT-B, and Verbal Fluency Test -fruits/vegetables compared with HCs. 5 key findings →
Participants: 104 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. 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% of the library) are not peer-reviewed — 962 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 →