Ten studies assessing retinal properties in dementia were included. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Ten studies assessing retinal properties in dementia were included. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
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PSMD is a new, fully automated, and robust imaging marker for SVD. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →
Design: longitudinal study Participants: 164 Evidence: moderate
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Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+. 1 key finding →
Design: cohort study Participants: 174 Evidence: moderate
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Autosomal-dominant AD is associated with increased WMH well before expected symptom onset. 4 key findings →
Participants: 299 Evidence: low
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Thirty-eight (68%) patients who consented to PET imaging had PS-MCI. 5 key findings →
Design: prospective cohort Participants: 178 Evidence: moderate
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There were minimal effects of lifestyle enrichment on AD biomarker trajectories (specifically rates). 5 key findings →
Design: longitudinal study Participants: 393 Evidence: moderate
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The FAD cortical signature appears to be similar to that described for sporadic AD. 5 key findings →
Design: longitudinal study Participants: 43 Evidence: moderate
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Researchers used a tau PET agent to examine tau retention patterns in cognitively normal older people and compared them with young controls and Alzheimer's disease patients. 3 key findings →
Evidence: low
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The goal of this paper was to evaluate the in vivo kinetics of the novel tau-specific PET radioligand 18 F-AV-1451 in cognitively healthy control (HC) and Alzheimer disease (AD) subjects, using reference region analyses. 2 key findings →
Design: longitudinal study Participants: 43 Evidence: moderate
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There is considerable debate whether Alzheimer's disease (AD) originates in basal forebrain or entorhinal cortex. 1 key finding →
Design: longitudinal study Evidence: moderate
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Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV-1451 binding and suggests complexity in AV-1451 binding. 4 key findings →
Participants: 38 Evidence: low
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The surface area of inclusion bodies increased as a function of cortical amyloid burden. 4 key findings →
Design: cohort study Evidence: moderate
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Medial temporal lobe AV-1451 uptake distinguishes AD dementia from probable DLB, which may be useful for differential diagnosis. 3 key findings →
Participants: 19 Evidence: moderate
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Idiopathic rapid eye movement (REM) sleep behaviour disorder (IRBD) manifests as unpleasant dreams and vigorous behaviours during REM sleep that can result in injuries. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression. 2 key findings →
Participants: 20 Evidence: low
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Increased Aβ burden was observed in TBI. 2 key findings →
Evidence: low
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There is a close, but not obligatory, association between logopenic PPA and AD. 3 key findings →
Participants: 19 Evidence: low
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Amyloidosis in the absence of neurodegeneration did not have an adverse impact on practice effects or the 30-month cognitive trajectories. 5 key findings →
Design: longitudinal study Evidence: moderate
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This study provides evidence for heterogeneous pathologic substrates and possibly different pathophysiologic mechanisms underlying MRI-observed cortical microbleeds in the context of advanced CAA and Alzheimer disease. 1 key finding →
Evidence: low
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Idiopathic rapid eye movement sleep behaviour disorder is characterized by nocturnal violence, increased muscle tone during rapid eye movement sleep and the lack of any other neurological disease. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
WMH volume within the inferior fronto-occipital fasciculus (IFOF) was the highest among all tract ROIs and associated with reduced FC in IFOF-connected DMN areas, independently of global AV-45 PET. 3 key findings →
Participants: 78 Evidence: low
Full summary, score breakdown and related studies → Original source
This diagnosis, based on clinical and MRI findings, suggests that vascular lesions lead to depression by disruption of frontal-subcortical-limbic networks involved in mood regulation. 3 key findings →
Evidence: low
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We report kinetic modeling results of dynamic acquisition data from 0 to 100 min after injection with the tau PET tracer 18 F-AV-1451 in 19 subjects. 2 key findings →
Participants: 19 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. 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 →