Amyloid beta (Aβ) plaque is a defining pathologic feature of Alzheimer disease (AD). 5 key findings →
Design: case report Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid beta (Aβ) plaque is a defining pathologic feature of Alzheimer disease (AD). 5 key findings →
Design: case report Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
As potential harbingers of future cognitive decline, physicians should query and monitor SMCs from their older patients. 1 key finding →
Participants: 531 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In women, increased plasma adiponectin levels are an independent risk factor for the development of both all-cause dementia and AD. 3 key findings →
Design: cohort study Participants: 159 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings enhance understanding of AD risk factors by relating validated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic variation at the APP locus in the earliest, presymptomatic stages of AD. 4 key findings →
Participants: 114 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Nearly half of all adults older than 60 years of age report sleep disturbance, as characterised either by reports of insomnia complaints with daytime consequences, dissatisfaction with sleep quality or quantity, or the diagnosis of insomnia disorder. 5 key findings →
Evidence: low
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Our data suggest that [F-18]-AV-1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1451 off-target binding. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Niney-two PD patients developed dementia, and 48 remained cognitively normal. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It was possible to assign all patients to one of the PD stages. 2 key findings →
Participants: 88 Evidence: moderate
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Frontotemporal lobar degeneration (FTLD) is the umbrella term encompassing a heterogeneous group of pathological disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Elevated CSF tau levels are associated with AD pathology and can help discriminate AD from other dementing disorders. 3 key findings →
Participants: 74 Evidence: moderate
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This study of a large series of community-based incident dementia cases provides a way of judging the adequacy of currently available clinical diagnostic criteria. 2 key findings →
Participants: 134 Evidence: low
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Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV-1451 binding and suggests complexity in AV-1451 binding. 4 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
18 F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Senile plaques are a prominent pathological feature of Alzheimer's disease (AD), but little is understood about the association of glial cells with plaques or about the dynamics of glial responses through the disease course. 2 key findings →
Participants: 91 Evidence: low
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Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We examined regional distribution patterns of phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) intraneuronal inclusions in frontotemporal lobar degeneration (FTLD). 1 key finding →
Participants: 39 Evidence: low
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Level of cognitively stimulating activity in old age is related to risk of developing dementia. 4 key findings →
Participants: 90 Evidence: low
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Longitudinal clinicopathologic cohort study. 1 key finding →
Design: cohort study Evidence: moderate
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LBD patients with AD copathology harbor greater neocortical SYN pathology. 1 key finding →
Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The blood-brain barrier (BBB) keeps neurotoxic plasma-derived components, cells, and pathogens out of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. 1 key finding →
Evidence: low
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Abnormal intracellular protein aggregates comprise a key characteristic in most neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% 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 →