Our results suggest that DTI data provide better prediction accuracy than GM volume in predementia AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our results suggest that DTI data provide better prediction accuracy than GM volume in predementia AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegeneration status was correctly identified in 78.8% (119/151) of amyloid-negative patients through visual rating, compared to 67.5% (102/151) using logistic regression. 5 key findings →
Participants: 379 Evidence: low
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Alzheimer's disease (AD) and frontotemporal dementia (FTD) are the most burdensome neurodegenerative disorders in older populations as they pose significant challenges because of subtle cognitive decline in the initial stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Until recently, accurate early detection of clinical symptoms associated with Alzheimer's disease (AD) and related dementias (ADRD) has been difficult. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Neural Network classifier achieved an accuracy of 91% with a 95% CI ranging from 0.79-0.97 and an AUC of 94%, on the test set after identifying the most significant features for AD prediction. 5 key findings →
Participants: 174 Evidence: low
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Alzheimer’s disease (AD) is a slow-growing neurological disorder that destroys human thought and consciousness. 1 key finding →
Evidence: low
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Alzheimer’s disease (AD) is a neurodegenerative disorder that affects millions of people worldwide. 3 key findings →
Evidence: low
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IntroductionThe prevalence of neurodegenerative diseases has significantly increased, necessitating a deeper understanding of their symptoms, diagnostic processes, and prevention strategies. 2 key findings →
Design: narrative review Evidence: low
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Alzheimer's dementia (AD) is a degenerative brain disease characterized by a decline in cognitive function and memory. 1 key finding →
Design: longitudinal study Evidence: moderate
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Thioflavin T derivatives are used in positron-emission tomography (PET) studies to detect amyloid protein deposits in patients with Alzheimer disease. 2 key findings →
Evidence: low
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Brain PET adds value in diagnosing neurodegenerative disorders, especially frontotemporal dementia (FTD) due to its syndromic presentation that overlaps with a variety of other neurodegenerative and psychiatric disorders. 18F-FDG-PET has improved sensitivity and specificity compared with structural MR imaging, with optimal diagnostic results achieved when both techniques are utilized. 2 key findings →
Evidence: low
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Successful back-translating clinical biomarkers and molecular imaging methods of Alzheimer's disease (AD), including positron emission tomography (PET), are very valuable for the evaluation of new therapeutic strategies and increase the quality of preclinical studies. 18 F-Fluorodeoxyglucose (FDG)-PET and 18 F-Florbetaben-PET are clinically established biomarkers capturing two key pathological features of AD. 3 key findings →
Evidence: low
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Region specific correlations between corpus callosum size and EEG coherence suggest that the decline in interhemispheric connectivity in Alzheimer's disease results from a specific loss of cortical association neurones projecting through the corpus callosum. 3 key findings →
Evidence: low
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All recently approved monoclonal antibodies (eg, aducanumab, lecanemab, and donanemab) for Alzheimer disease (AD) were shown to increase the risks of amyloid-related imaging abnormalities (ARIA) in randomized clinical trials, which can include brain swelling or hemorrhage. 4 key findings →
Participants: 240 Evidence: high
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Early and accurate prognosis of Alzheimer’s disease (AD) remains limited by current biomarkers, which are often invasive, require expensive equipment, or fail to predict individual trajectories of cognitive decline. 2 key findings →
Participants: 459 Evidence: moderate
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Fourteen studies met eligibility criteria, covering populations from healthy controls to individuals with subjective cognitive decline, MCI, AD, and other dementias. 5 key findings →
Evidence: low
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[18F]GTP1 exhibited retention patterns that correlated with [18F]PI-2620 and [18F]MK-6240 for all Braak regions (except Braak II). 4 key findings →
Evidence: low
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Alzheimer\\\'s disease (AD), the leading cause of dementia worldwide, affects more than 55 million individuals and gen-erates annual healthcare costs exceeding two trillion USD [14]. 5 key findings →
Design: longitudinal study Evidence: moderate
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Utilizing machine learning, we identify a 12-protein panel from cerebrospinal fluid proteomic datasets. 5 key findings →
Evidence: low
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Accurate classification of neurodegenerative disorders remains a challenge in neuroscience. 3 key findings →
Evidence: low
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Both (18)F-FDG and (11)C-PiB imaging appear to be of limited use for predicting the progression from MCI to dementia due to AD in short-term follow-up, irrespective of the strategy of analysis. 3 key findings →
Evidence: low
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Participants’ motivations for testing and long-term adaptation to the results were strongly shaped by cognitive concerns and personal experiences of dementia in relatives. 5 key findings →
Participants: 17 Evidence: moderate
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The Boston v2.0 criteria have low accuracy in patients with AD dementia. 1 key finding →
Participants: 63 Evidence: moderate
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AD patients had significantly higher AD-RAI (0.91 ± 0.25) and more pronounced hippocampal atrophy (0.36 ± 0.09) compared to MCI and HC (P 0.9 for distinguishing BPSD from non-BPSD patients. 3 key findings →
Participants: 40 Evidence: low
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Accurate differentiation of Alzheimer's disease (AD), frontotemporal dementia (FTD), and healthy control (HC) is critical for early diagnosis and intervention of brain disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 →