A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD). 4 key findings →
Participants: 62 Evidence: low
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.
Although a link between body mass index (BMI) and brain volume has been established in several cross-sectional studies, evidence of the association between change in BMI over time and changes in brain structure is limited. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The s allele variant of the serotonin transporter gene (5-HTT) has recently been observed to moderate the relationship of stress to depression and anxiety. 5 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Different patterns of regional brain atrophy were found among patients of different APOE genotypes. 1 key finding →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Early to mid-adolescence is an important developmental period for subcortical brain maturation, but longitudinal studies of these neurodevelopmental changes are lacking. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Temporoparietal hypoperfusion on SPECT is common to both AD and DLB. 2 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that different subcortical areas have different vulnerabilities to ischemia in CADASIL. 4 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain cell-derived small extracellular vesicles (sEVs) in blood offer unique cellular and molecular information related to the onset and progression of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Reduction in CSF Abeta(42), likely reflecting Abeta aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive deficits and depression appear to be more common in aging former NFL players compared with healthy controls. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular contributions to cognitive impairment are increasingly recognized 1-5 as shown by neuropathological 6,7 , neuroimaging 4,8-11 , and cerebrospinal fluid biomarker 4,12 studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]AV-1451 binds to tau in AD, and some other tauopathies. 2 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Animal studies demonstrate that hyperactive neurons facilitate early accumulation and spread of tau and amyloid-β proteins in the pathological cascade of Alzheimer's disease (AD). 3 key findings →
Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source
Clear divergence in tauopathy between the sexes are apparent approximately 20 years earlier than previously reported. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
LPA is associated with Abeta amyloidosis, suggesting that subclassification of PPA based on language features can help predict the likelihood of AD pathology. 3 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
There is a strong relationship between beta-amyloid deposition and atrophy very early in the disease process. 2 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
PET imaging with (11)C-labeled Pittsburgh Compound-B ((11)C-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD). 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Volumetric magnetic resonance imaging analyses of 30 subjects were undertaken to quantify the global and temporal lobe atrophy in semantic dementia and Alzheimer's disease. 2 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
This study demonstrates a disruption of whole-brain topological organization of the functional connectome in aMCI. 3 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
This study suggests that amyloid load is significantly raised in over 80% of subjects with DLB, while amyloid pathology is infrequent in PDD. 5 key findings →
Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Primary biomarker efficacy endpoints were not statistically significant in either dose group. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Aducanumab is the first FDA-approved amyloid-lowering immunotherapy for Alzheimer's disease. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Monoclonal antibodies targeting amyloid-β are the first approved disease-modifying treatment for Alzheimer’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is no consensus for a blood-based test for the early diagnosis of Alzheimer's disease (AD). 3 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 2,885 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.
- Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging
- Prediabetes as a critical stage for risk of dementia and stroke: evidence from the UK Biobank and Mendelian randomization.:evidence from the UK Biobank and Mendelian Randomization
- Predicting White Matter Hyperintensity: Leveraging Portable MRI for Accessible Brain Health Screening
- The neuropsychological profile of vascular cognitive impairment in stroke and TIA patients
- Mediterranean diet and magnetic resonance imaging-assessed cerebrovascular disease
- Cognitive decline and brain volume loss as signatures of cerebral amyloid-beta peptide deposition identified with Pittsburgh compound B: cognitive decline associated with Abeta deposition
- Concurrent Changes in Plasma Phosphorylated Tau 217, Tau PET, and Cognition in Preclinical Alzheimer Disease
- Visual Versus Fully Automated Analyses of 18F-FDG and Amyloid PET for Prediction of Dementia Due to Alzheimer Disease in Mild Cognitive Impairment
- In vivo retention of 18F-AV-1451 in corticobasal syndrome
- Clinicopathological characterization of vacuolar tauopathy associated with VCP D395G
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 →