We extend prior work using BAG from sporadic AD to ADAD, noting consistent results. 5 key findings →
Evidence: moderate
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.
We extend prior work using BAG from sporadic AD to ADAD, noting consistent results. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinicians reported high diagnostic confidence in 83% of 18 F-FDG PET compared to 67% for CBF-SPECT (P = 0.001). 2 key findings →
Participants: 126 Evidence: low
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Tau spatial spread may demonstrate earlier changes than tau burden which could have broad impact in clinical trial design. 1 key finding →
Design: cross-sectional Evidence: low
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These findings suggest that APOE genotype has a differential effect on the distribution of amyloid plaques and glucose metabolism. 2 key findings →
Evidence: low
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Lecanemab is a humanized monoclonal antibody that is selective for soluble amyloid-beta (Aβ) aggregates. 1 key finding →
Evidence: high
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White matter abnormalities on magnetic resonance imaging (MRI) are associated with dementia and include white matter hyperintensities (WMH; also termed leukoaraiosis) and visible perivascular spaces (PVS). 2 key findings →
Evidence: low
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Patchy subcortical foci of increased signal intensity are frequently identified on magnetic resonance imaging (MRI) in the elderly. 2 key findings →
Evidence: low
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Changes in PCC functional connectivity comprised bidirectional alterations in the resting networks in AD-affected brains, and the impaired resting functional connectivity seemed to change with AD progression. 1 key finding →
Evidence: low
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18 F-PI-2620 showed peak brain uptake around 5 min after injection and fast washout from nontarget regions. 5 key findings →
Evidence: low
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Studies suggest a link between bone loss and Alzheimer's disease. 3 key findings →
Participants: 71 Evidence: low
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The discordant topography between atrophy and hypometabolism reported in AD is already present at the aMCI stage. 4 key findings →
Participants: 20 Evidence: low
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Clinical, neuropsychological, and imaging profiles can contribute to accurate antemortem diagnosis in FTD. 3 key findings →
Evidence: low
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A 7-min window, corresponding to minutes 1-8 (frames 5-15), produced the highest voxelwise correlation between (18)F-FDG and pPIB (R = 0.78 ± 0.05). 4 key findings →
Evidence: moderate
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Atrophy of the CC differentiates HE and ID from AD subjects and tracks the cognitive decline of this disease. 4 key findings →
Design: cross-sectional Evidence: moderate
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The association of neurofibrillary tangles with delayed verbal recall may reflect associated hippocampal atrophy. 2 key findings →
Evidence: low
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Resting state functional magnetic resonance imaging (fMRI) was used to measure whole brain functional connectivity within specific networks hypothesised to be more affected in dementia with Lewy bodies (DLB) (a disease characterised by prominent attentional deficits, spontaneous motor features of parkinsonism and depression) than in Alzheimer׳s disease (AD) and controls. 4 key findings →
Participants: 68 Evidence: low
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Impaired ability to conduct daily activities is a diagnostic criterion for dementia and a determinant of healthcare services utilization and caregiver burden. 4 key findings →
Evidence: low
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Rey's Auditory Verbal Learning Test (RAVLT) is a powerful neuropsychological tool for testing episodic memory, which is widely used for the cognitive assessment in dementia and pre-dementia conditions. 2 key findings →
Evidence: low
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We used a previously validated automated machine learning algorithm based on adaptive boosting to segment the hippocampi in baseline and 12-month follow-up 3D T1-weighted brain MRIs of 150 cognitively normal elderly (NC), 245 mild cognitive impairment (MCI) and 97 Dementia of the Alzheimer's type (DAT) ADNI subjects. 3 key findings →
Evidence: low
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These findings lay groundwork to enable AD clinical trials with characterization and disease-specific tracking of DS adults. 3 key findings →
Evidence: low
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This well-characterized case of PCA syndrome due to AD in a very young patient with DS demonstrates the occurrence of atypical presentations in DS that might be overshadowed by the baseline intellectual disability associated with DS. 5 key findings →
Evidence: low
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The role of hypoperfusion in Alzheimer's disease (AD) is a vital component to understanding the pathogenesis of this disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical hallmark of Alzheimer's disease (AD) is a gradual decline in cognitive function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In vivo [ 18 F]-AV-1451 PET neuroimaging was performed in 5 patients with sporadic CJD (median age, 66 years [63-74]), and results were compared to cognitively normal (CN) persons (n = 44; median age, 68 years [63-74]) and to participants with very mild Alzheimer disease (AD) dementia (n = 8; median age, 77 years [63-90]). 4 key findings →
Participants: 44 Evidence: low
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Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) may have overlapping clinical presentations despite distinct underlying neuropathologies, thus making in vivo diagnosis challenging. 4 key findings →
Participants: 185 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 2,885 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 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 →