Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER. 2 key findings →
Design: cross-sectional Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid chronicity provides unique information about cognitive decline and neurofibrillary tangle development and may be useful to investigate preclinical Alzheimer's disease. 2 key findings →
Design: longitudinal study Participants: 257 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subtraction MRI has potential as a visual aid increasing the sensitivity of ARIA-E assessment. 3 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design. 2 key findings →
Design: cohort study Participants: 276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
69/100
Primary include several amyloid PET measurements (Centiloid, SUVr, BPND , R1 ), and secondary are their changes from baseline, relationship to other amyloid markers (cerebrospinal fluid and visual assessment), and predictive value of AD-related decline. 2 key findings →
Design: cohort study Participants: 2,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions. 1 key finding →
Design: longitudinal study Participants: 867 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Twelve articles-published between the 2007 and 2017-have been included in this systematic review after a quantitative and qualitative selection. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Although brain neuroinflammation may play an instrumental role in the pathophysiology of Alzheimer's disease, its actual impact on disease progression remains controversial, being reported as either detrimental or protective. 4 key findings →
Design: longitudinal study Participants: 33 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We found that a higher PGS was associated with higher rates of tau-PET accumulation, in particular at elevated amyloid-PET levels. 4 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
53/310 (17.1%) subjects were classified as Focal-FMM. 5 key findings →
Design: longitudinal study Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 641 participants with CSF Aβ42 data and at least two 18F-florbetapir scans, 335 (52.3%) were male. 4 key findings →
Design: cohort study Participants: 402 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline. 1 key finding →
Design: cohort study Participants: 110 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Florbetapir-PET imaging was performed a mean of 99 days (range, 1-377 days) before death for the 29 individuals in the primary analysis cohort. 2 key findings →
Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Thinning in specific cortical areas known to be affected by Alzheimer disease (AD) is detectable in individuals with questionable AD dementia (QAD) and predicts conversion to mild AD dementia. 3 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We tested the trained model using five other studies, three of which used PET as a biomarker of significant amyloid β burden (testing the deep learning model between amyloid β positive vs amyloid β negative). 2 key findings →
Design: case-control study Participants: 648 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Accumulating evidence demonstrates that metabolic changes in the brain associated with neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in the pathophysiology of mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. 5 key findings →
Design: longitudinal study Participants: 32 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
Principal component analysis identified patterns of variation in baseline and longitudinal measures of tau uptake and volume that were significantly different across phenotypes. 2 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85). 3 key findings →
Design: cross-sectional Participants: 118 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The (11)C-PiB-PET imaging results demonstrated reduction of fibrillar Aβ accumulation in patients with Alzheimer disease treated with bapineuzumab; however, as no clinical benefit was observed, the findings are consistent with the hypotheses that bapineuzumab may not have been initiated early enough in the disease course, the doses were insufficient, or the most critical Aβ species were inadequately targeted. 4 key findings →
Design: clinical trial Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a multi-center study assessing neuroimaging in diagnosis and longitudinal monitoring. 4 key findings →
Design: longitudinal study Participants: 339 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal studies will be required to determine the association of elevated [(11)C]PIB binding and risk of developing dementia of the Alzheimer type. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In clinically normal older adults, lower functional connectivity predicted more rapid decline in PACC scores over time, particularly when coupled with increased Aβ burden. 2 key findings →
Design: longitudinal study Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 1,159 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.
- Explainable machine learning for predicting longitudinal dementia status: Establishing a leakage-free benchmark
- Clinical use of amyloid-positron emission tomography neuroimaging: Practical and bioethical considerations
- Amyloid imaging with (18)F-florbetaben in Alzheimer disease and other dementias
- A Cohort Study on Alzheimer's Disease in Relation to Residential Magnetic Fields From Indoor Transformer Stations
- Brain amyloid imaging
- Discriminative Plasma Lipidomic Signatures of Dementia with Lewy Bodies and Alzheimer’s Disease: A Targeted Mass Spectrometry and Machine Learning Approach
- Biomarker Investigation Using Multiple Brain Measures from MRI Through Explainable Artificial Intelligence in Alzheimer’s Disease Classification
- Sex and age differences in atrophic rates: an ADNI study with n=1368 MRI scans
- Brain beta-amyloid measures and magnetic resonance imaging atrophy both predict time-to-progression from mild cognitive impairment to Alzheimer's disease
- Using positron emission tomography and florbetapir F18 to image cortical amyloid in patients with mild cognitive impairment or dementia due to Alzheimer disease
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 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.
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 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 →