The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study's findings suggest that PET imaging with [18F]flortaucipir could be used to identify the density and distribution of AD-type tau pathology and the presence of high levels of AD neuropathological change, supporting a neuropathological diagnosis of AD. 4 key findings →
Participants: 64 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ADNI has demonstrated the feasibility and utility of multicenter PET studies and is helping to clarify the role of biomarkers in the study of aging and dementia. 3 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
67/100
Florbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the brains of living subjects. 4 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by a decline in cognitive functions with no validated disease modifying treatment. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We investigated the effect of crenezumab, a humanized anti-amyloid-beta (Aβ) immunoglobulin (Ig)G4 monoclonal antibody, on biomarkers of amyloid pathology, neurodegeneration, and disease progression in patients with mild-to-moderate Alzheimer's disease (AD). 4 key findings →
Participants: 26 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Reference region selection has an important influence on the detection of florbetapir change. 4 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
44 participants were included: 20 PSEN1 E280A mutation carriers and 24 non-carriers. 2 key findings →
Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
For one of the primary analyses, the interpretation of the florbetapir scans (majority interpretation of five nuclear medicine physicians, who classified each scan as amyloid positive or amyloid negative) was compared with amyloid pathology (assessed according to the Consortium to Establish a Registry for Alzheimer's Disease standards, and classed as amyloid positive for moderate or frequent plaques or amyloid negative for no or sparse plaques); correlation of the image analysis results with amyloid burden was tested as a coprimary endpoint. 3 key findings →
Participants: 59 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In mostly small single-center studies, Alzheimer's disease (AD) is associated with characteristic and progressive reductions in fluorodeoxyglucose positron emission tomography (PET) measurements of the regional cerebral metabolic rate for glucose (CMRgl). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tensor-based morphometry (TBM) is a powerful method to map the 3D profile of brain degeneration in Alzheimer's disease (AD) and mild cognitive impairment (MCI). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Infant ε4 carriers had lower MWF and GMV measurements than noncarriers in precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions, areas preferentially affected by AD, and greater MWF and GMV measurements in extensive frontal regions and measurements were also significant in the subset of 2- to 6-month-old infants (MWF differences, P Conclusions and relevance While our findings should be considered preliminary, this study demonstrates some of the earliest brain changes associated with the genetic predisposition to AD. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It introduces criteria to determine whether an image is associated with an intermediate-to-high likelihood of pathologic AD or with having any identifiable cortical amyloid level above that seen in low-risk young controls. 3 key findings →
Participants: 46 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Florbetapir F18 has been approved by the Food and Drug Administration for in vivo assessment of amyloid pathology in patients undergoing evaluation for Alzheimer disease (AD). 3 key findings →
Participants: 229 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is a major neurodegenerative disease and the most common cause of dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Interest in understanding the roles of white matter (WM) inflammation and damage in the pathophysiology of Alzheimer disease (AD) has been growing significantly in recent years. 5 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The groups of individuals who agreed to participate in the imaging substudies of AD trials were remarkably comparable to the comparison groups at baseline on a wide range of demographic and clinical measures; there seems to be a minimal effect of self-selection bias. 4 key findings →
Participants: 166 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This study compared FDG-PET and clinical measurements in elderly subjects with memory disturbance to examine relationships between glucose metabolism and cognitive or functional scores. 3 key findings →
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 30,580 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events