28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) and frontotemporal dementia (FTD) are leading causes of cognitive decline. 4 key findings →
Design: cross-sectional Evidence: low
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Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →
Evidence: low
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The differential diagnosis of frontotemporal dementia (FTD) and Alzheimer's disease (AD) is difficult due to the overlaps of clinical symptoms. 4 key findings →
Participants: 47 Evidence: low
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The subject groups for model derivation comprised 80 healthy subjects (HS), 36 patients with mild cognitive impairment (MCI) who converted to AD dementia within 18 months, 85 non-converter MCI patients who did not convert within 24 months, and 67 AD dementia patients with baseline FDG PET scan were recruited from the AD Neuroimaging Initiative (ADNI) database. 4 key findings →
Participants: 36 Evidence: moderate
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The neurological deterioration associated with Alzheimer's disease (AD), involving accumulation of amyloid-beta peptides and neurofibrillary tangles, is associated with evident neuroinflammation. 4 key findings →
Evidence: moderate
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Data from 17 107 individuals (321 Asian, 635 Black, 829 Hispanic, and 15 322 White) with MCI or dementia and amyloid PET were analyzed between April 2020 and January 2022. 5 key findings →
Design: cohort study Participants: 3,154 Evidence: moderate
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This comprehensive review examines the integration of Quantitative Electroencephalography (qEEG) and Artificial Intelligence (AI) in the detection and diagnosis of Alzheimer's Disease (AD). 5 key findings →
Participants: 890 Evidence: low
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The proportion of false negatives from FDG-PET ranged from 11-55%. 5 key findings →
Design: longitudinal study Participants: 112 Evidence: moderate
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Alzheimer’s disease (AD), a leading neurodegenerative disorder, progresses from an intermediary stage known as Mild Cognitive Impairment (MCI), characterized by measurable cognitive decline with retained functional independence. 1 key finding →
Design: longitudinal study Evidence: moderate
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< 0.001). Shape features demonstrated the highest predictive accuracy for conversion, with areas under the curve of 0.891 at baseline and 0.898 at 2 years. 5 key findings →
Design: longitudinal study Participants: 180 Evidence: moderate
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Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques. 3 key findings →
Design: longitudinal study Participants: 127 Evidence: moderate
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Aggregated TDP-43 is a hallmark of frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and limbic-predominant age-related TDP-43 encephalopathy (LATE), and a common co-pathology in other neurodegenerative diseases. 5 key findings →
Evidence: low
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The FCAAS-4 achieved a mean area under the receiver operating characteristic curve (AUC-ROC) of 0.74 (95% confidence interval: 0.71-0.77) and a Harrell generalized c-index of 0.72 (0.70-0.75). 5 key findings →
Design: cohort study Evidence: moderate
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Researchers evaluated twenty-one patients diagnosed with MCI using PET studies with (11)C-PIB and (18)F-fluoro-deoxy-glucose (FDG), cognitive assessments, and CSF sampling. 3 key findings →
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[18F]flutemetamol PET scans were positive in 133 out of 211 (63%) patients, of whom 110 out of 144 (76%) patients had a pre-PET Alzheimer's disease (AD) diagnosis and 23 out of 67 (34%) patients had a non-AD diagnosis. 5 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
On the basis of the independent validation dataset, the 18 F-FDG PET model yielded a significantly higher predictive value than the amyloid PET model. 5 key findings →
Participants: 159 Evidence: low
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Amyloid imaging with PET and measuring cortical thickness with MRI are suitable biomarkers to detect disease progression in early AD within a small sample. 3 key findings →
Design: longitudinal study Evidence: moderate
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A subset of a dementia subgroup with characteristics predominantly associated with DM-related factors may underlie a pathophysiology different from AD, although these patients were clinically diagnosed as having AD. 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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Pseudotemporal measurements from baseline PET data explained 87% ( P Pseudotemporal analysis of baseline PET images is capable of predicting the regional pattern of longitudinal Aβ accumulation in AD at a group level. 3 key findings →
Design: longitudinal study Participants: 58 Evidence: moderate
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These findings indicate EXT may be more sensitive to Aβ's role in preclinical AD than level and improve targeting of individuals for AD prevention trials. 2 key findings →
Evidence: low
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Development of molecular imaging agents for fibrillar β-amyloid positron-emission tomography during the past decade has brought molecular imaging of Alzheimer disease pathology into the spotlight. 1 key finding →
Design: cohort study Evidence: moderate
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Alzheimer's disease is characterized both by a lower mean level of functional connectivity as well as by diminished fluctuations in the level of synchronization. 2 key findings →
Participants: 24 Evidence: low
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There is no evidence for individual risk prediction and even less for specific treatments. 5 key findings →
Evidence: moderate
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Magnetic resonance imaging-based volumetric measurements provide a useful technique for quantifying in vivo regional cerebral atrophy in Alzheimer disease (AD). 3 key findings →
Evidence: low
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Amyloid-related imaging abnormalities (ARIA) is a term introduced in 2010 to encompass a spectrum of MRI findings observed in patients receiving investigational anti-amyloid beta (Aβ) immunotherapies for Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 1,160 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →