Both Aβ and tau pathology affect default mode network integrity before clinical onset of Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloidosis in the absence of neurodegeneration did not have an adverse impact on practice effects or the 30-month cognitive trajectories. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Deposition of iron in the brain is proposed to play a role in the pathophysiology of the normal aging process and neurodegenerative diseases. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
SUVr(60-90) and SUVr(40-60) overestimated binding with 13% and 10%, respectively, compared with RPM2. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinical stages showed a progressively increased prevalence of Aβ-positivity and higher entorhinal tau PET pathology from cognitively normal (CN) to SOCD, MCI, and dementia in both tracers. 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
50/100
The AI-powered pipeline achieved robust performance with intraclass correlation coefficients exceeding 0.97 for regional uptake estimation compared with MR-based ground truth. 5 key findings →
Design: longitudinal study Participants: 666 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The results suggest that (11)C-PIB binding to Aβ deposits in transgenic mouse brain is highly dependent on the AD model and the structure of its Aβ plaques. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
O]water PET were strongest for 1800 msec single-PLD and generally decreased with longer PLDs, except the occipital lobe, where all PLDs showed poor agreement. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Eighty-three Black (mean 72±10.8-years-old, 63% female, 33% cognitively impaired) and 27 Latino participants (mean 65.8-years-old, 56% female, 11% cognitively impaired) completed neuroimaging. 5 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease staging from structural magnetic resonance imaging (MRI) is challenging when clinically adjacent stages and severe class imbalance are considered simultaneously. 2 key findings →
Design: longitudinal study Participants: 3,592 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Thirty-two patients met the inclusion criteria (n=11 moderate-to-severe SVD, mean age 72 ± 10 years, 6 women; n = 21 none-to-minimal SVD, mean age 70 ± 10 years, 12 women). 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
16% of individuals were identified as tau-accumulators. 5 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These results provide clear evidence that CU older adults with both amyloid plaques and tau aggregates measured with PET will develop cognitive impairments if the disease is not stopped. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Spatial analyses localised early hippocampal tau-PET signal predominantly to the anterior CA1. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Progressive cortical thinning in multiple cognition-related regions was significantly associated with cBF atrophy. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer\\\'s disease (AD), the leading cause of dementia worldwide, affects more than 55 million individuals and gen-erates annual healthcare costs exceeding two trillion USD [14]. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitively normal older adults are often regarded as a homogeneous population in preventive and disease-modifying clinical trials for dementia. 2 key findings →
Design: prospective cohort Participants: 1,136 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BACKGROUNDPeople with type 2 diabetes mellitus (T2DM) are at higher risk of cerebral small vessel disease and left ventricular hypertrophy (LVH), potentially contributing to cognitive decline and dementia. 5 key findings →
Design: cohort study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundDeep-learning models predict mild cognitive impairment (MCI)-to-Alzheimers disease (AD) conversion from structural MRI with high accuracy. 1 key finding →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Greater baseline WMH burden was associated with differential longitudinal progression in converters across eleven clinical outcomes, including cognition, gait, and functional independence (all q<0.05). 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
16/100
BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases. 5 key findings →
Design: longitudinal study Participants: 1,091 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Compared with controls, adjusted odds of classification into a more impaired CDR category were higher in all tiers (OR 2.55-5.08, 95% CI 1.22-11.34). 1 key finding →
Design: longitudinal study Participants: 343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
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 29,380 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.
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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% 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 →