Inexpensive, non-invasive tools for assessing Alzheimer-type pathophysiologies are needed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Inexpensive, non-invasive tools for assessing Alzheimer-type pathophysiologies are needed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD. 5 key findings →
Evidence: low
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Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments. 5 key findings →
Evidence: low
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Alzheimer disease (AD) primarily affects older adults. 5 key findings →
Design: case report Evidence: low
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In this study, we aimed to compare cerebrospinal fluid (CSF) levels of total tau (t-tau), phosphorylated tau (p-tau(181)) and positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) in the differential diagnosis of Alzheimer's disease (AD) under clinical conditions. 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
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The analyses of the community‐based U.S. POINTER indicate that AA/B individuals present differences in AD and related dementia biomarker values. nHW had higher fully adjusted cognitive scores. 5 key findings →
Participants: 644 Evidence: low
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We studied with functional magnetic resonance imaging (fMRI) differences in resting-state networks between patients with mesial temporal lobe epilepsy (MTLE) and healthy subjects. 3 key findings →
Evidence: low
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Contrary to expectations, high versus low ADI groups only showed a difference in hippocampal volume, but in the reverse direction. 4 key findings →
Participants: 310 Evidence: low
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In 4 of 5 patients treated with lecanemab or donanemab and who had moderate or severe ARIA-E, Aβ PET signal decreased significantly more in regions that had been involved with ARIA-E. Greater regional Aβ PET signal reduction in areas involved by ARIA-E may reflect enhanced local Aβ clearance, reduced tracer binding site availability, impaired glymphatic flow from immune complex deposition, or other mechanisms. 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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The fMRI entropy classifier matched the tau PET model in accuracy and outperformed it in F1 score (0.64 vs. 0.61) and area under the curve (AUC; 0.73 vs. 0.67). 4 key findings →
Evidence: moderate
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BackgroundTo date, cholinomimetics remain central in the pharmacotherapy of Alzheimer's disease (AD) dementia. 2 key findings →
Evidence: low
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In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics. 4 key findings →
Participants: 70 Evidence: low
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The model incorporating age, brain volume, functional, and radiomics features demonstrated the highest predictive performance for SCD progression in training (C-index: 0.962; 95 % CI: 0.95-0.98) and testing (C-index: 0.911; 95 % CI: 0.861-0.968) sets. 5 key findings →
Participants: 89 Evidence: low
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The mean hippocampal volumes were significantly smaller in the DEM group compared to the MCI and healthy groups (P <0.0001). 5 key findings →
Participants: 22 Evidence: low
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Alcohol use disorder (AUD) is linked with changes in brain structure and function, with robust evidence for neurodegenerative changes, including synaptic loss in preclinical models. 2 key findings →
Evidence: low
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The MIND diet may buffer the cognitive consequences of cerebrovascular pathology and cortical atrophy in older adults at elevated dementia risk and promote cognitive resilience over general healthy eating guidelines. 2 key findings →
Design: post-hoc analysis Evidence: low
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Delirium exhibited a metabolic profile of network dysfunction that may be modifiable and clinically responsive. 4 key findings →
Evidence: low
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Our data suggests that microglial reactivity may play a role in hippocampal atrophy; potentially contributing to the increasingly recognized interaction between vascular and neurodegenerative pathology. 3 key findings →
Evidence: low
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Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America. 1 key finding →
Evidence: low
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Positron emission tomography (PET) allows for minimally invasive in vivo localization of amyloid and tau deposition, and visualization of glucose metabolism using amyloid PET, tau PET, and FDG PET. 1 key finding →
Participants: 58 Evidence: low
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Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment. 1 key finding →
Evidence: low
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Three robustly differentiated AD subtypes (S1, S2, and S3) were identified, with 93% validation accuracy and Adjusted Mutual Information scores >0.89, each exhibiting distinct tau patterns. 5 key findings →
Design: cross-sectional Evidence: low
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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.
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →