Each measure independently predicted a diagnosis of dementia. 1 key finding →
Participants: 2,885 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Longitudinal changes in motor function may be useful in the early detection of dementia during preclinical stages, when the utility of disease-modifying therapies would be greatest. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
60/100
Neuroimaging and biofluid tau markers hold potential for optimising such clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with behavioural Alzheimer's disease showed worse memory scores than behavioural variant frontotemporal dementia and did not differ from typical Alzheimer's disease, while executive function composite scores were lower compared to behavioural variant frontotemporal dementia and typical Alzheimer's disease. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Different biomarkers for Alzheimer disease provide different information from one another that is likely to be complementary. 1 key finding →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Linking the ADAMS dementia clinical assessment data to the wealth of available longitudinal HRS data on health, health care utilization, informal care, and economic resources and behavior, will provide a unique opportunity to study the onset of CIND and dementia in a nationally representative population-based sample, as well as the risk factors, prevalence, outcomes, and costs of CIND and dementia. 5 key findings →
Design: longitudinal study Participants: 856 Evidence: moderate
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Prevalence of dementia was 8.3%. 2 key findings →
Design: cross-sectional Participants: 1,238,895 Evidence: low
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60/100
We aimed to determine the regional pattern of brain atrophy associated with the C9ORF72 gene mutation, and to determine which regions best differentiate C9ORF72 from subjects with mutations in tau and progranulin, and from sporadic frontotemporal dementia. 5 key findings →
Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The diagnostic accuracy for MSA was suboptimal in this autopsy study. 3 key findings →
Participants: 134 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Long-term use of sulfonylureas, thiazolidinediones, or insulin was not associated with an altered risk of developing AD. 3 key findings →
Design: case-control study Evidence: moderate
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These findings support previous contentions that a "preclinical phase" of detectable cognitive deficits can precede the clinical diagnosis of probable AD by many years, and they also support the hypothesis that problems with secondary verbal memory are among the first signs of AD. 4 key findings →
Design: longitudinal study Participants: 1,045 Evidence: moderate
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Incomplete penetrance was suggested in two kindreds, and the youngest generation had significantly earlier age of onset (>10 years) compared with the next oldest generation in 11 kindreds. 2 key findings →
Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study aim was to describe the temporal course of cognitive decline in Alzheimer's disease (AD). 1 key finding →
Design: longitudinal study Participants: 226 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
As expected, the MENO group was older than the PERI and CNT groups. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
60/100
The cross-sectional difference in 2 independent neuroimaging modalities indicates early AD pathology in SMI. 2 key findings →
Design: cross-sectional Participants: 31 Evidence: moderate
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We found no significant correlation between CSF biomarkers and cognitive scores in any of the 3 clinical groups individually. 2 key findings →
Design: cross-sectional Participants: 399 Evidence: low
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In a middle-aged, at-risk cohort, a physically active lifestyle is associated with an attenuation of the deleterious influence of age on key biomarkers of AD pathophysiology. 3 key findings →
Design: cross-sectional Participants: 186 Evidence: high
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Compared with noncarriers, cognitively unimpaired mutation carriers had elevated mean cortical Pittsburgh Compound B distribution volume ratio levels in their late 20s, and 7 of 9 carriers older than 30 years reached the threshold for amyloidosis (distribution volume ratio level > 1.2). 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
60/100
Iron concentration in the deep gray matter and neocortical regions was higher in patients with Alzheimer disease than in healthy control participants. 3 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
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Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD. 2 key findings →
Design: cross-sectional Participants: 79 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ARIA-E can also occur spontaneously in cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with increased CSF levels of anti-Aβ autoantibodies. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
23% of the total global burden of disease is attributable to disorders in people aged 60 years and older. 5 key findings →
Evidence: low
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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →