27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
One of the most challenging problems in modern neuroimaging is detailed characterization of neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
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In this longitudinal study of 77 patients with mild cognitive impairment (MCI), the authors analyzed whether levels of tau protein phosphorylated at threonine 231 (p-tau(231)) in CSF correlate with progression of cognitive decline. 1 key finding →
Design: longitudinal study Participants: 77 Evidence: moderate
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The pathologic changes of Alzheimer disease (AD) evolve very gradually over decades before the disease becomes clinically manifest. 2 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
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The lack of effective predictors of the rate of dementia progression extends to the very earliest stages of the disease, including what is often called MCI. 1 key finding →
Design: longitudinal study Participants: 289 Evidence: moderate
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Depressive symptoms in MCI appear to be predictors for progression to AD. 3 key findings →
Design: longitudinal study Participants: 74 Evidence: moderate
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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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This study evaluated longitudinal CSF biomarker measures collected when participants were cognitively normal to determine the magnitude and time course of biomarker changes before the onset of clinical symptoms in subjects with mild cognitive impairment (MCI). 4 key findings →
Design: longitudinal study Participants: 265 Evidence: moderate
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At baseline, participants (n = 168) were cognitively normal and primarily middle-aged (mean 56.4 years, SD 10.9 years) and had both vascular risk factor status and proximal CSF biomarkers available. 4 key findings →
Design: cohort study Participants: 168 Evidence: moderate
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Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
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New technology is convenient for measuring blood total tau concentrations and provides a unique and increased opportunity for early intervention to slow cognitive decline. 4 key findings →
Design: cohort study Participants: 1,159 Evidence: moderate
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Because of the aging population and a rise in the number of stroke survivors, the prevalence of post-stroke cognitive impairment (PSCI) is increasing. 4 key findings →
Design: cohort study Participants: 280 Evidence: moderate
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Cognitive dysfunction, including dementia and delirium, is prevalent in geriatric emergency department (ED) patients, but often remains undetected. 4 key findings →
Design: cohort study Participants: 163 Evidence: moderate
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Delirium is a profound neuropsychiatric disturbance precipitated by acute illness. 4 key findings →
Design: longitudinal study Participants: 465 Evidence: moderate
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The 59 recruiting sites for the Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Design: cohort study Participants: 177 Evidence: moderate
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We recruited 825 individuals from the CHARLS sample and 766 subjects from hospitals in six provinces and cities in China. 4 key findings →
Design: longitudinal study Participants: 825 Evidence: moderate
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Cognitive impairment is one of the earliest, most common, and most disabling non-motor symptoms in Parkinson's disease (PD). 4 key findings →
Design: cohort study Participants: 360 Evidence: moderate
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Several studies suggested that women are at higher risk of dementia than men. 4 key findings →
Design: cohort study Participants: 7,046 Evidence: moderate
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Although memory complaints are associated with an increased risk of Alzheimer's disease in persons with cognitive impairment as well as in persons with normal cognition, they are commonly considered of less importance than objective cognitive measures. 4 key findings →
Design: cohort study Participants: 7,983 Evidence: moderate
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Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments. 4 key findings →
Design: longitudinal study Participants: 389 Evidence: moderate
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Plasma proteins affect biological processes and are common drug targets but their role in the development of Alzheimer's disease and related dementias remains unclear. 4 key findings →
Design: cohort study Evidence: moderate
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From the population-based Rotterdam Study, 4,447 participants underwent dietary assessment and brain MRI scanning between 2005 and 2015. 4 key findings →
Design: longitudinal study Participants: 4,447 Evidence: moderate
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White matter hyperintensities (WMHs) are commonly assumed to represent non-specific cerebrovascular disease comorbid to neurodegenerative processes, rather than playing a synergistic role. 4 key findings →
Design: longitudinal study Participants: 571 Evidence: moderate
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Recent studies have associated immune abnormalities with dementia. 4 key findings →
Design: longitudinal study Participants: 50,864 Evidence: moderate
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Whether the association of cardiovascular diseases (CVDs) with dementia differs by sex remains unclear, and the role of socioeconomic, lifestyle, genetic, and medical factors in their association is unknown. 4 key findings →
Design: cohort study Participants: 502,649 Evidence: moderate
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A total of 3,162 cases of dementia occurred during the follow-up. 5 key findings →
Design: cohort study Participants: 49,511 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 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 →