No adverse events occurred over the study period. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study performed an anatomical parcellation of the MNI spatially normalized single-subject high-resolution T1 volume by delineating main sulci as landmarks to define 45 anatomical volumes of interest (AVOI) in each hemisphere. 4 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Currently established and employed biomarkers of Alzheimer's disease (AD) predominantly mirror AD-associated molecular and structural brain changes. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A statistically significant yearly decline in hippocampal volume and an increase in temporal horn volume was identified in elderly control subjects who represent typical aging individuals. 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
We used multinomial regression models to estimate discrimination [concordance (C) statistics] among three amyloid PET stages (low, intermediate, high), four tau PET stages (Braak 0, 1-2, 3-4, 5-6) and a combined amyloid and tau PET stage (none/low versus intermediate/high severity) using plasma biomarkers as predictors separately within unimpaired and impaired individuals. 5 key findings →
Participants: 1,136 Evidence: low
Full summary, score breakdown and related studies → Original source
57/100
The CSF Aβ42/40 ratio is superior to Aβ42 alone as a marker of amyloid-positivity by PET. 3 key findings →
Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MPP-Aβ might be one of the potential blood biomarkers for the prediction of PiB-PET positivity in the brain. 2 key findings →
Design: cross-sectional Participants: 353 Evidence: low
Full summary, score breakdown and related studies → Original source
At a group-wise level, observable rates of short-term serial tau accumulation were only seen in the presence of abnormal amyloid. 5 key findings →
Participants: 126 Evidence: low
Full summary, score breakdown and related studies → Original source
Our baseline and 2-year imaging findings are compatible with a biphasic trajectory of inflammation in Alzheimer's disease: MCI cases with low baseline but subsequently rising β-amyloid load show correlated levels of microglial activation which then later decline when the β-amyloid load approaches AD levels. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
57/100
In Alzheimer's disease (AD), the Braak staging scheme suggests a stereotypical tau spreading pattern that does, however, not capture interindividual variability in tau deposition. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
MRI can also be used to assess comorbid vascular pathology and define homogeneous groups for inclusion or for subject stratification. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
All assays distinguished amyloid-positive from -negative individuals with high accuracy (89%-95%). 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher body mass index at baseline was correlated with lower levels of plasma phosphorylated tau (p-tau)217, p-tau217 ratio, neurofilament light chain (NfL), glial fibrillary acidic protein, and CLs. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the GAAIN dataset, the universal mask led to a small reduction in the variance of the YC, and a small increase in the inter-tracer agreement. 5 key findings →
Participants: 147 Evidence: moderate
Full summary, score breakdown and related studies → Original source
57/100
We found a consistent amyloid PET × age interaction on global tau PET increase in men (ADNI/A05: p = 0.0078/0.018), with younger men showing faster amyloid-associated tau accumulation. 5 key findings →
Participants: 301 Evidence: low
Full summary, score breakdown and related studies → Original source
18F-MK-6240 (18F-labeled 6-(fluoro)-3-(1H-pyrrolo[2,3-c]pyridin-1-yl)isoquinolin-5-amine) is a highly selective, subnanomolar-affinity PET tracer for imaging neurofibrillary tangles (NFTs). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The analytic sample included 469 participants (mean age 71.2 ± 8.5 years, 53% female). 3 key findings →
Design: cohort Participants: 469 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
We selected the cerebellum as a pseudo-reference region based on the immunohistochemical comparison of age-matched PS2APP and WT mice. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
D-CAA M + showed greater age-dependent FLR PiB retention (p - , and serially imaged asymptomatic M + demonstrated greater longitudinal increases (p = 0.004). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
PIB-positive subjects with mild cognitive impairment (MCI) are significantly more likely to convert to AD than PIB-negative patients, faster converters having higher PIB retention levels at baseline than slower converters. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amyloid β subgroups did not differ for any psychobehavioural, cognitive, actigraphy, and structural and functional neuroimaging results after adjustment for age, sex, and level of education More participants positive for amyloid β deposition had the APOE ε4 allele (33 [38%] vs 29 [13%], p 1-42 concentration in CSF significantly correlated with mean 18 F-florbetapir uptake at baseline (r=-0·62, p 1-42 to amyloid β 1-40 (r=-0·61, p 18 F-florbetapir uptake at baseline (mean standard uptake value ratio 1·46 [SD 0·16] vs 1·02 [SD 0·20]), and more were carriers of the APOE ε4 allele (three [75%] of four vs 33 [39%] of 83). 1 key finding →
Participants: 318 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The deep-learning time-to-event model predicted individual subjects' progression to AD dementia with a concordance index of 0.762 on 439 Alzheimer's Disease Neuroimaging Initiative testing MCI subjects with follow-up duration from 6 to 78 months (quartiles: [24, 42, 54]) and a concordance index of 0.781 on 40 Australian Imaging Biomarkers and Lifestyle Study of Aging testing MCI subjects with follow-up duration from 18 to 54 months (quartiles: [18, 36, 54]). 2 key findings →
Participants: 2,146 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We present evidence of AD-induced changes in global brain functional connectivity specifically affecting long-distance connectivity. 2 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
56/100
Among patients with cognitive symptoms, larger choroid plexus volume was associated with severity of cognitive impairment in the Alzheimer disease spectrum. 5 key findings →
Participants: 532 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia and Alzheimer disease display different spatial distributions of hypoperfusion on arterial spin labeling MRI. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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.
- Amyloid PET predicts longitudinal functional and cognitive trajectories in a heterogeneous cohort
- Alzheimer disease predicting from clinical and MRI data using DeepALZNET dual pathway framework
- A review of the flortaucipir literature for positron emission tomography imaging of tau neurofibrillary tangles
- Clinical Relevance of [18F]Florbetaben and [18F]FDG PET/CT Imaging on the Management of Patients with Dementia
- Clinical significance of focal ß-amyloid deposition measured by 18F-flutemetamol PET
- Concordance between Centiloid Quantification and Visual Interpretation of Amyloid PET Scans across the Alzheimer Disease Continuum
- Quantitative assessment of synaptic density in the outer molecular layer of the hippocampal dentate gyrus in Alzheimer's disease
- Amyloid PET and cognitive decline in cognitively normal individuals: the SCIENCe project
- Small-animal PET imaging of amyloid-beta plaques with [11C]PiB and its multi-modal validation in an APP/PS1 mouse model of Alzheimer's disease
- Abnormal amplitude of low-frequency fluctuations of intrinsic brain activity in Alzheimer's 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 →