28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 1018 study patients enrolled, 508 were randomly assigned to rivastigmine and 510 to placebo; 17.3% of patients on rivastigmine and 21.4% on placebo progressed to AD (hazard ratio 0.85 [95% CI 0.64-1.12]; p=0.225). 4 key findings →
Evidence: high
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A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer's disease (AD) dementia. 2 key findings →
Participants: 340 Evidence: low
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Among Aβ-positive individuals, greater CR related to attenuated clinical progression in predementia stages of AD, but accelerated cognitive decline after the onset of dementia. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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Elecsys CSF biomarker assays may provide reliable alternatives to PET in Alzheimer's disease diagnosis. 3 key findings →
Participants: 277 Evidence: moderate
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The SCIENCe study confirms that SCD is a heterogeneous group, with preclinical AD and subthreshold psychiatric features. 4 key findings →
Design: cohort study Participants: 114 Evidence: moderate
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Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI. 5 key findings →
Design: longitudinal study Participants: 186 Evidence: moderate
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Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →
Evidence: low
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The models could aid clinicians in the interpretation of CSF biomarker and hippocampal volume results in individuals with MCI, and help research and clinical settings to prepare for a future of precision medicine in Alzheimer's disease. 1 key finding →
Participants: 883 Evidence: moderate
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Whether or not neuropsychiatric symptoms (NPS) in advance of dementia are associated with Alzheimer's disease (AD) and/or other neurodegenerative dementias remains to be determined. 5 key findings →
Participants: 1,016 Evidence: low
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Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time. 2 key findings →
Design: cross-sectional Evidence: moderate
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PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers. 3 key findings →
Participants: 400 Evidence: low
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(n = 16,683) had an average age of 69.07 ± 7.34, 72.04% were female, and had an average of 16.66 ± 2.26 years of education. 5 key findings →
Design: longitudinal study Participants: 16,683 Evidence: moderate
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Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769 Evidence: low
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Most approaches to machine learning from electronic health data can only predict a single endpoint. 1 key finding →
Participants: 1,909 Evidence: low
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The diagnostic guidelines of Alzheimer's disease (AD) have recently been updated to include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient has an ongoing AD neuropathologic process or not. 3 key findings →
Design: cross-sectional 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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Baseline plasma NfL was associated with increased risk of dementia/death in the entire cohort. 4 key findings →
Design: longitudinal study Participants: 131 Evidence: moderate
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By fitting Cox proportional hazards models, we find that baseline model stage is a significant risk factor for conversion from both mild cognitive impairment to Alzheimer's disease (P = 2.06 × 10(-7)) and cognitively normal to mild cognitive impairment (P = 0.033). 2 key findings →
Evidence: low
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Because it is a potentially modifiable metabolic state, with multiple peripheral and central targets for intervention, it may represent a target for alleviating parkinsonian symptoms and slowing progression to disability and dementia. © 2022 The Authors. 2 key findings →
Evidence: low
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Alzheimer's disease is characterized by the histopathological presence of amyloid-β plaques and tau-containing neurofibrillary tangles. 3 key findings →
Evidence: low
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Significant progress has been made in understanding the pre-symptomatic phase of amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
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Our data suggest that structural MRI can be used to identify biologically and clinically meaningful subtypes of AD. 3 key findings →
Evidence: low
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When an individual with MCI-LB endorsed more clinical features, they typically experienced a faster cognitive decline (ACE-R Score Difference β = -1.1 [-1.7 to -0.5]), specifically when experiencing visual hallucinations (β = -2.1 [-3.5 to -0.8]) or cognitive fluctuations (β = -3.4 [-4.8 to -2.1]).Individuals with MCI-LB typically acquired more clinical features with the passage of time (25.5% [20.0-32.0%] one-year probability), limiting the prognostic utility of baseline-only features. 3 key findings →
Design: cohort study Participants: 74 Evidence: moderate
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Deposits of abnormally phosphorylated tau protein are found in numerous neurodegenerative disorders; the 'tauopathies', which include Alzheimer's and Pick's diseases, but tau pathology is also found in the ageing brain. 2 key findings →
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →