Our study supports the usefulness of [ 18 F]AV1451 to characterize tau pathology in at least a subset of pathogenic MAPT mutations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our study supports the usefulness of [ 18 F]AV1451 to characterize tau pathology in at least a subset of pathogenic MAPT mutations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Concluding, this innovative EEG analysis, in combination with a genetic test (both low-cost and widely available), could evaluate on an individual basis with great precision the risk of MCI progression. 3 key findings →
Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD). 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies of autosomal dominant Alzheimer disease (AD) have shown structural and cognitive changes in mutation carriers decades prior to clinical disease. 1 key finding →
Participants: 717 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
APOEε4 is the most well-established genetic risk factor for sporadic Alzheimer's disease and is associated with cerebral amyloid-β. 4 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
Defects in phospholipase A(2) lead to a range of phenotypes. 4 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
DTI histograms may be used as an adjunct outcome measure in future therapeutic trials. 1 key finding →
Design: longitudinal study Evidence: moderate
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Major imaging biomarkers of Alzheimer's disease include amyloid deposition [imaged with [(11)C]Pittsburgh compound B (PiB) PET], altered glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
[18F]Flortaucipir BPND images showed overall highest binding in the symptomatic carriers. 5 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to APOE ε4 non-carriers, APOE ε4 carriers had lower rsFC in temporal DMN, but only in non-Hispanic Whites. 3 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source
Amnestic forms of MCI appear to have demographic, genetic, and MRI findings suggestive of Alzheimer disease pathology, whereas the nonamnestic forms of MCI have findings suggestive of vascular disease. 4 key findings →
Design: cross-sectional Participants: 153 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is a close, but not obligatory, association between logopenic PPA and AD. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The E693Delta mutation has been suggested as a cause of dementia because of enhanced formation of synaptotoxic Abeta oligomers. 2 key findings →
Participants: 2,121 Evidence: low
Full summary, score breakdown and related studies → Original source
As of 2023, it is estimated that 6.7 million individuals in the United States live with Alzheimer's disease (AD). 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
The lack of fibrillar β-amyloid (Aβ) as visualized by PiB PET in APParc mutation carriers suggests, given the reduced glucose metabolism and levels of Aβ(1-42) in CSF, that other forms of Aβ such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Light-to-moderate alcohol intake is associated with a lower prevalence of vascular brain findings and, in APOE epsilon4 carriers, hippocampal and amygdalar atrophy on MRI. 3 key findings →
Participants: 509 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multiple lines of evidence suggest that specific subtypes of age-related cataract (ARC) and Alzheimer disease (AD) are related etiologically. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The retina, an anatomical extension of the brain, forms physiological connections with the visual cortex of the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is one of several proteins associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE ε4 showed significant (P < .05) associations with tau deposition across all disease stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our analyses demonstrate lower retinal capillary densities in early disease, in cognitively normal APOE ε4 gene carriers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Northwestern University SuperAging Project recruits community dwellers over the age of 80 who have unusually high performance on tests of episodic memory. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hereditary diseases are caused by mutations in genes, and more than 7,000 rare diseases affect over 30 million Americans. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study indicates that, as a group, GBA mutation-positive individuals show a deterioration in clinical markers consistent with the prodrome of PD. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →