30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dementia and MCI are associated with neuropsychiatric symptoms in clinical samples. 4 key findings →
Design: cohort study Participants: 138 Evidence: moderate
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We found that distinct sphingolipid species including sphingomyelin (SM) with acyl residue sums C16:0, C18:1, and C16:1 (SM C16:0, SM C18:1, SM C16:1) and hydroxysphingomyelin with acyl residue sum C14:1 (SM (OH) C14:1) were consistently associated with severity of AD pathology at autopsy and AD progression across prodromal and preclinical stages. 5 key findings →
Design: longitudinal study Participants: 44 Evidence: moderate
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The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. 3 key findings →
Design: meta-analysis Participants: 3,154 Evidence: high
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Among older women, those with sleep-disordered breathing compared with those without sleep-disordered breathing had an increased risk of developing cognitive impairment. 4 key findings →
Design: cross-sectional Participants: 60 Evidence: low
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Early identification of patterns of abnormality is of fundamental importance for detecting disease onset and tracking progression. 2 key findings →
Design: longitudinal study Participants: 1,017 Evidence: moderate
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In this study, lower AD signature region volumes, brain microhemorrhages, higher WMH volumes, and infarcts were risk factors associated with dementia in older community-based residents. 4 key findings →
Design: cohort study Participants: 1,553 Evidence: moderate
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
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Neuropsychiatric symptoms in MCI are associated with significantly an increased risk of incident dementia and AD. 5 key findings →
Design: cohort study Participants: 1,821 Evidence: moderate
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This study provides evidence for sex differences in the progression to cognitive impairment in PD, while specific cognitive features become more important indicators of progression with impending conversion to PDD. 3 key findings →
Design: longitudinal study Participants: 418 Evidence: moderate
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Diabetes increased the risk of conversion to dementia. 2 key findings →
Design: meta-analysis Evidence: high
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The development of MCI is associated with measurements of cognition and depression, racial and constitutional factors, and cerebrovascular disease. 5 key findings →
Design: longitudinal study Participants: 927 Evidence: moderate
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From October 2018 to March 2020, 58 participants were recruited (29 per group, 95% [86%-99%]). 5 key findings →
Design: randomized controlled trial Participants: 58 Evidence: high
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This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study Participants: 271 Evidence: moderate
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These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. 5 key findings →
Design: longitudinal study Participants: 274 Evidence: moderate
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AD-signature cortical thinning in CN-AD converters in both samples was remarkably similar, about 0.2 mm (p 1). 3 key findings →
Design: longitudinal study Evidence: moderate
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Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Participants: 139 Evidence: moderate
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This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
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Diabetes status, poor glycemic control, and longer diabetes duration were associated with worse cognitive outcomes over a median follow-up of 5 years. 4 key findings →
Participants: 5,099 Evidence: low
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It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI). 4 key findings →
Design: cohort study Participants: 185 Evidence: moderate
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From a longitudinal study of normal (Clinical Dementia Rating [CDR] = 0; n = 77) and mildly impaired (CDR = 0.5; n = 167) participants with 5 or more annual clinical assessments, baseline level of cognitive impairment in daily life was graded using CDR sum of boxes (CDR-SB) and level of cognitive performance impairment was graded using neuropsychological test scores. 4 key findings →
Design: longitudinal study Participants: 77 Evidence: moderate
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The First Key Symposium was held in Stockholm, Sweden, 2-5 September 2003. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is a syndrome thought to be a prodrome of dementia for some patients. 4 key findings →
Design: longitudinal study Participants: 1,379 Evidence: moderate
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Neither targeted lecanemab treatment nor treatment unrestricted by APOE ε4 genotype is cost-effective vs SoC alone for patients with MCI or mild dementia due to AD. 2 key findings →
Design: modelling Evidence: moderate
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The field of aging and dementia is focusing on the characterization of the earliest stages of cognitive impairment. 1 key finding →
Evidence: low
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Pooling data across 4 cohort studies, 814 cognitively normal participants (mean baseline age = 59.6 years) were classified into 8 ATN groups using baseline CSF levels of β-amyloid 1-42 as a measure of amyloid (A), phosphorylated tau 181 as a measure of tau (T), and total tau as a measure of neurodegeneration (N). 4 key findings →
Design: cohort study Evidence: moderate
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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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →