27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The purpose of this study was to use serial imaging to gain insight into the sequence of pathologic events in Alzheimer's disease, and the clinical features associated with this sequence. 3 key findings →
Design: longitudinal study Participants: 21 Evidence: moderate
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In clinical samples, people with amnestic MCI are at high risk of developing Alzheimer's disease dementia, with annual rates of progression from MCI to Alzheimer's disease estimated at approximately 10% to 15% compared with the base incidence rates of Alzheimer's disease dementia of 1% to 2% per year. 5 key findings →
Design: cohort study Participants: 33 Evidence: moderate
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11 studies were identified, including 380 patients with AD, 68 with MCI and 293 healthy controls (HC). 4 key findings →
Design: meta-analysis Participants: 380 Evidence: high
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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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However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. 5 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
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We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex. 5 key findings →
Design: longitudinal study Evidence: moderate
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The 52 baseline participants comprised autosomal dominant Alzheimer's disease mutation carriers (n = 11; 49.6 ± 10.3 years old) and non-carriers (n = 16; 51.1 ± 14.2 years old; 10 male), and patients with sporadic mild cognitive impairment (n = 17; 61.9 ± 6.4 years old; nine male) and sporadic Alzheimer's disease (n = 8; 63.0 ± 6.5 years old; five male); for confidentiality reasons, the gender of mutation carriers is not revealed. 3 key findings →
Design: longitudinal study Evidence: moderate
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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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This fifteen-year study provides a large database of highly characterized individuals with longitudinal cognitive, imaging and lifestyle data and biofluid collections, to aid in the development of interventions to delay onset, prevent or treat AD. 1 key finding →
Design: cohort study Participants: 1,112 Evidence: moderate
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We set out to determine factors that influence the rate of brain atrophy in 1-year longitudinal magnetic resonance imaging (MRI) data. 1 key finding →
Design: longitudinal study Participants: 363 Evidence: moderate
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See Coulthard and Knight (doi:10.1093/aww335) for a scientific commentary on this article. 1 key finding →
Design: longitudinal study Participants: 530 Evidence: moderate
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Plasma Abeta42/Abeta40 ratio has potential as a prescreener to identify Alzheimer pathological changes in cognitively normal individuals with SCD. 2 key findings →
Participants: 248 Evidence: moderate
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The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. 1 key finding →
Design: longitudinal study Participants: 551 Evidence: moderate
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We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods. 3 key findings →
Participants: 165 Evidence: low
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A high percentage of patients with mild cognitive impairment (MCI) develop clinical dementia of the Alzheimer type (AD) within 1 year. 3 key findings →
Design: longitudinal study Evidence: moderate
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Capturing the dynamics of gray matter (GM) atrophy in relation to the conversion from mild cognitive impairment (MCI) to clinically probable Alzheimer's disease (AD) would be of considerable interest. 3 key findings →
Design: longitudinal study Evidence: moderate
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Tensor-based morphometry can recover three-dimensional longitudinal brain changes over time by nonlinearly registering baseline to follow-up MRI scans of the same subject. 2 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
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A challenge in developing informative neuroimaging biomarkers for early diagnosis of Alzheimer's disease is the need to identify biomarkers that are evident before the onset of clinical symptoms, and which have sufficient sensitivity and specificity on an individual patient basis. 4 key findings →
Design: longitudinal study 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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Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %). 5 key findings →
Design: longitudinal study Participants: 1,136 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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Neuropsychiatric symptoms (NPSs) are common in patients with Alzheimer's disease (AD) and are associated with accelerated cognitive impairment and earlier deaths. 2 key findings →
Evidence: low
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To accurately predict the development of Alzheimer's disease (AD) at its predementia stage would be a major breakthrough from both therapeutic and research standpoints. 5 key findings →
Design: longitudinal study Evidence: moderate
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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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Our work shows that peripheral differential methylation between age-matched subjects with AD relative to healthy controls will provide opportunities to further investigate and validate differential methylation as a surrogate of disease. 2 key findings →
Design: longitudinal study Participants: 653 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →