28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
A major unanswered question in the dementia field is whether cognitively unimpaired individuals who harbor both Alzheimer's disease neuropathological hallmarks (that is, amyloid-β plaques and tau neurofibrillary tangles) can preserve their cognition over time or are destined to decline. 3 key findings →
Participants: 1,325 Evidence: low
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Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. 2 key findings →
Design: longitudinal study Participants: 62 Evidence: moderate
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Fifty-one AD patients enrolled, mean age 73.5. 4 key findings →
Design: clinical trial Evidence: high
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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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Accumulating evidence demonstrates that metabolic changes in the brain associated with neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in the pathophysiology of mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
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Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by a decline in cognitive functions with no validated disease modifying treatment. 1 key finding →
Design: cross-sectional Evidence: moderate
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These studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design. 2 key findings →
Design: longitudinal study Evidence: moderate
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Cross-sectional functional magnetic resonance imaging studies using a memory task in patients with mild cognitive impairment have produced discordant results, with some studies reporting increased hippocampal activity--consistent with findings in genetic at-risk populations--and other studies reporting decreased hippocampal activity, relative to normal controls. 3 key findings →
Design: cross-sectional Participants: 33 Evidence: moderate
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The most novel characteristics of our machine learning model compared to previous ones are the following: 1) our deep learning model is multi-tasking, in the sense that it jointly learns to simultaneously predict both MCI to AD conversion as well as AD vs. healthy controls classification, which facilitates relevant feature extraction for AD prognostication; 2) the neural network classifier employs fewer parameters than other deep learning architectures which significantly limits data-overfitting (we use ∼550,000 network parameters, which is orders of magnitude lower than other network designs); 3) both structural MRI images and their warp field characteristics, which quantify local volumetric changes in relation to the MRI template, were used as separate input streams to extract as much information as possible from the MRI data. 1 key finding →
Participants: 785 Evidence: low
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Compared to age matched controls, in the AD group, we found increases in both spectral power and coherence at the slower frequencies (Delta, Theta). 5 key findings →
Participants: 26 Evidence: low
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We used Cox proportional hazards models and logistic regressions to assess whether circadian disturbances predict an increased risk of incident Alzheimer's dementia and conversion of mild cognitive impairment to Alzheimer's dementia. 3 key findings →
Design: cohort study Evidence: moderate
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This text discusses the characterisation of subjective cognitive decline (SCD), a term conceived in 2014 to describe cognitively unimpaired individuals who are concerned about reduced cognitive function and seek medical help. 3 key findings →
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There is increasing evidence that subjective cognitive decline (SCD) in individuals with unimpaired performance on cognitive tests may represent the first symptomatic manifestation of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Structural magnetic resonance imaging data are frequently analysed to reveal morphological changes of the human brain in dementia. 3 key findings →
Design: longitudinal study Evidence: moderate
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Identification of potentially modifiable risk factors for cognitive deterioration is important. 5 key findings →
Participants: 5,607 Evidence: low
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Alzheimer's disease (AD) pathologies were discovered in the accessible neurosensory retina. 3 key findings →
Evidence: low
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PET can evaluate amyloid expansion from cortex to subcortex. 1 key finding →
Participants: 1,433 Evidence: low
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From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →
Design: longitudinal study Evidence: moderate
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ADNI participants (921 dyads) had a mean (SD) age of 71 (7) years and mean (SD) of 17 (3) years of education; 485 (53%) were female, 30 (3%) were Asian, 105 (11%) were Black, and 756 (82%) were White. eVAL participants (279 dyads) had a mean (SD) age of 71 (8) years and mean (SD) of 17 (2) years of education; 151 (54%) were female, 17 (6%) were Asian, 12 (4%) were Black, and 245 (88%) were White. 5 key findings →
Design: cross-sectional Participants: 921 Evidence: moderate
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ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →
Evidence: low
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The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials. 3 key findings →
Evidence: low
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The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD). 3 key findings →
Participants: 509 Evidence: low
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Sex differences in Alzheimer's disease (AD) biology and progression are not yet fully characterized. 2 key findings →
Evidence: low
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Pathological hallmarks of Alzheimer's disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. 4 key findings →
Participants: 13 Evidence: low
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Older adults with subjective cognitive decline (SCD) in the absence of objective neuropsychological dysfunction are increasingly viewed as at risk for non-normative cognitive decline and eventual progression to Alzheimer's disease (AD) dementia. 3 key findings →
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →