Rare variants should only be investigated in users with a family history of early-onset dementia in a first degree relative. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Rare variants should only be investigated in users with a family history of early-onset dementia in a first degree relative. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that correlating NLP and ASA with clinician observations is an objective and novel approach to measuring speech and language changes in neurodegenerative disorders. 2 key findings →
Participants: 30 Evidence: low
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Differences between predictors for dementia in younger old versus oldest old populations, as well as for dementia versus pathology, should be considered more carefully in future studies. 4 key findings →
Participants: 245 Evidence: moderate
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Isoprostanes and prostaglandins are biomarkers for oxidative stress and inflammation. 4 key findings →
Evidence: moderate
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It is largely unknown how alcohol use affects the risk of Alzheimer`s disease (AD). 4 key findings →
Design: cohort study Participants: 301 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation and synaptic degeneration are major neuropathological hallmarks in Alzheimer's disease (AD). 3 key findings →
Participants: 95 Evidence: low
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Previous research has described distinct subtypes of Alzheimer's disease (AD) based on the differences in regional patterns of brain atrophy on MRI. 4 key findings →
Evidence: low
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Plasma amyloid-β (Aβ) levels are increasingly studied as a potential accessible marker of cognitive impairment and dementia. 4 key findings →
Participants: 458 Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia, characterized by the accumulation of amyloid-beta (Aβ) and neurofibrillary tangles. 4 key findings →
Participants: 16 Evidence: low
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Dominance of 4R over three-repeat (exon 10-) tau isoforms contrasts with earlier reports of R406W patients and was not sufficiently explained by the presence of H1/H2 haplotypes in two of the autopsied patients. 3 key findings →
Design: systematic review Evidence: low
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Across studies, MBI appears to be linked to specific neurobiological markers of AD, including Aβ and tau brain deposition, as well as alterations in the mesolimbic pathway and neurodegenerative and neuroinflammatory fluid biomarker levels. 3 key findings →
Design: systematic review Evidence: high
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Patients with all biomarkers positive for AD (N = 145) had the highest hazard for progression to dementia due to AD, whilst patients with no positive biomarkers (N = 111) had the lowest. 3 key findings →
Participants: 145 Evidence: moderate
Full summary, score breakdown and related studies → Original source
NDs share a CSF profile characterized by increased levels of CSF CHIT1, YKL-40, and GFAP, which likely reflects a common neuroinflammatory response to protein misfolding and aggregation. 3 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
A primary goal of research in cognitive impairment and dementia is to understand how some individuals retain sufficient cognitive function for a fulfilling life while many others are robbed of their independence, sometimes their essence, in the last years and decades of life. 5 key findings →
Evidence: low
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Amyloid pathology is associated with changes in structural MRI measures in CN and MCI. 3 key findings →
Participants: 337 Evidence: low
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Applying an integrative multi-omics approach we report novel molecular and pathways alterations associated with AD pathology. 5 key findings →
Evidence: moderate
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Glymphatic dysfunction is a crucial pathway for dementia. 4 key findings →
Evidence: low
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There is accumulating evidence that synaptic loss precedes neuronal loss and correlates best with impaired memory formation in Alzheimer's disease (AD). 4 key findings →
Participants: 52 Evidence: low
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Our findings lend support to a model in which fibrillar Aβ is still accumulating in the early stages of clinical disease but approaching a relative plateau, a point at which Aβ may uncouple from neurodegenerative processes including synaptic loss. 5 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Multidomain intervention studies conducted so far appear to have mixed results and substantial variability in target populations, format and intensity of interventions, choice of control conditions, and outcome measures. 2 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source
We hypothesized that cerebrospinal fluid (CSF) biomarkers of amyloid, neurodegeneration, and endothelial dysfunction would differ between older African Americans and Caucasians with normal cognition and cognitive impairment associated with AD. 3 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings provide additional insight into gut microbial involvement in AD and add to the growing understanding of the gut-brain axis. 2 key findings →
Participants: 410 Evidence: low
Full summary, score breakdown and related studies → Original source
Abeta (1-42/1-40) and GFAP independently associated with amyloid PET status (p = 0.009 and p < 0.001 respectively), and GFAP and NfL independently associated with syndrome diagnosis (p = 0.001 and p = 0.048 respectively). 2 key findings →
Participants: 176 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid and positron emission tomography biomarkers accurately predict an underlying Alzheimer's disease (AD) pathology; however, they represent either invasive or expensive diagnostic tools. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Robust and accessible biomarkers that can capture the heterogeneity of Alzheimer's disease and its diverse pathological processes are urgently needed. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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