27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
This simple and feasible cognitive impairment prediction model could identify community-dwelling elderly people at the greatest 3-year risk for cognitive impairment, which could help community nurses in the early identification of dementia. 1 key finding →
Design: prospective cohort Evidence: moderate
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Virtually all adults with Down syndrome (DS) show the neuropathological changes of Alzheimer disease (AD) by the age of 40 years. 2 key findings →
Design: longitudinal study Evidence: moderate
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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Aβ40 levels changed less for the simvastatin group (not statistically significant). 4 key findings →
Design: cohort study Participants: 21 Evidence: high
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Women with MCI have greater longitudinal rates of cognitive and functional progression than men. 2 key findings →
Design: longitudinal study Evidence: moderate
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Interferon-gamma-inducible protein 10 is specifically increased in MCI and seems to decrease with the progression of AD, whereas MCP-1 and IL-8 are up-regulated also in late stages of the disease, suggesting a role in phases in which neurodegeneration is prevalent. 3 key findings →
Design: longitudinal study Participants: 36 Evidence: moderate
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The NIA-AA criteria apply to most MCI subjects in both the community and clinical trials settings; however, a sizeable proportion of subjects had conflicting biomarkers, which may be very important and need to be explored. 2 key findings →
Design: longitudinal study Evidence: moderate
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Hippocampal atrophy, posterior cingulate and frontal glucose hypometabolism, and white-matter tract disruption are well described early macroscopic events in Alzheimer's disease. 2 key findings →
Design: longitudinal study Evidence: moderate
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Risk factors for progression from MCI to probable AD differed in men and women. 5 key findings →
Design: cohort study Participants: 294 Evidence: moderate
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Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) 1 . 4 key findings →
Design: longitudinal study Evidence: moderate
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Biomarkers have become increasingly important in understanding neurodegenerative processes associated with Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 116 Evidence: moderate
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Compare cognitive and hippocampal volume trajectories in asymptomatic middle-aged and older adults with positive CSF markers of β-amyloid (Aβ) or tau to adults without an Alzheimer disease (AD)-associated biomarker profile. 4 key findings →
Design: cohort study Participants: 78 Evidence: moderate
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We investigated the effects of matrix type and reagent batch changes on diagnostic performances and longitudinal trajectories of brain-derived tau (BD-tau). 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
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We sought to develop and evaluate a composite memory score from the neuropsychological battery used in the Alzheimer's Disease (AD) Neuroimaging Initiative (ADNI). 4 key findings →
Design: longitudinal study Evidence: moderate
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In mostly small single-center studies, Alzheimer's disease (AD) is associated with characteristic and progressive reductions in fluorodeoxyglucose positron emission tomography (PET) measurements of the regional cerebral metabolic rate for glucose (CMRgl). 4 key findings →
Design: longitudinal study Evidence: moderate
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One hundred and twenty-six patients diagnosed with Alzheimer-type dementia were selected from among 200 consecutive outpatients evaluated for suspected dementia from 1980 to 1982. 4 key findings →
Design: cohort study Participants: 126 Evidence: moderate
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Cerebrospinal fluid (CSF) levels of Abeta peptide 1-42 (Abeta 42), tau, and phosphorylated tau (ptau) are potential biomarkers of Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
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Chronic obesity is associated with several complications, including cognitive impairment and dementia. 4 key findings →
Design: cohort study Evidence: moderate
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We propose a new method of measuring atrophy of brain structures by simultaneously segmenting longitudinal magnetic resonance (MR) images. 4 key findings →
Design: longitudinal study Participants: 206 Evidence: moderate
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To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Design: longitudinal study Participants: 1,184 Evidence: moderate
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Setting and participants A total of 316,669 participants [mean (SD) age, 56.3 (8.1) years] without prior cardiovascular disease or dementia from the UK Biobank study at baseline survey (2006-2010) were enrolled. 4 key findings →
Design: cohort study Participants: 316,669 Evidence: moderate
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We included 730 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants without dementia (282 cognitively normal, 448 mild cognitive impairment) with baseline [ 18 F]florbetapir PET and CSF Aβ 42 available. 4 key findings →
Design: longitudinal study Participants: 318 Evidence: moderate
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The relationship between mild behavioral impairment (MBI) and Alzheimer's disease (AD) is intricate and still not well investigated. 4 key findings →
Design: longitudinal study Participants: 1,129 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 →