Mutations in presenilin 2 are rare causes of early onset familial Alzheimer's disease. 4 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mutations in presenilin 2 are rare causes of early onset familial Alzheimer's disease. 4 key findings →
Participants: 64 Evidence: low
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Our data suggest that cardiovascular risk factors may modulate the clinical expression of CADASIL. 5 key findings →
Design: prospective cohort Evidence: moderate
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The role of the Alzheimer's Disease Neuroimaging Initiative Genetics Core is to facilitate the investigation of genetic influences on disease onset and trajectory as reflected in structural, functional, and molecular imaging changes; fluid biomarkers; and cognitive status. 5 key findings →
Design: longitudinal study Evidence: moderate
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Different information sources yield widely varied prevalence and expenditure estimates. 1 key finding →
Participants: 57,669 Evidence: low
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Risk of overall dementia and its subtypes was not associated with MetS or any MetS component in participants younger than 75. 4 key findings →
Participants: 749 Evidence: moderate
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Commonly used organophosphate and organochlorine pesticides inhibit acetylcholinesterase at synapses in the somatic, autonomic, and central nervous systems and may therefore have lasting effects on the nervous system. 2 key findings →
Evidence: low
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Changes in CSF biomarker levels may identify early neurodegenerative processes of Alzheimer disease. 2 key findings →
Design: longitudinal study Evidence: moderate
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This study suggests that larger head circumference is associated with less cognitive impairment in the face of cerebral atrophy. 3 key findings →
Design: cross-sectional Participants: 270 Evidence: low
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Forty-eight patients were randomized to treatment with either topiramate or risperidone, and 41 patients (21 of 25 in topiramate group and 20 of 23 in risperidone group) completed the trial. 4 key findings →
Participants: 41 Evidence: high
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Doubly dissociated areas of hypoperfusion in FTLD and AD are consistent with areas of significant histopathologic burden in these groups. 5 key findings →
Participants: 18 Evidence: low
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Our study showed an association between neurofibrillary pathology and frontal PVWMH and DWMH (rather than parietal), as a surrogate of small vessel disease, particularly in very old community-dwelling individuals. 5 key findings →
Participants: 132 Evidence: moderate
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Frailty is a risk for postoperative complications and an independent predictor of in-hospital mortality, institutional discharge, and reduced midterm survival. 1 key finding →
Participants: 3,826 Evidence: low
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Machine learning and pattern recognition methods have been used to diagnose Alzheimer's disease (AD) and mild cognitive impairment (MCI) from individual MRI scans. 3 key findings →
Evidence: low
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Among adults with DS, decreasing levels of plasma Aβ42, a decline in the Aβ42/Aβ40 ratio, or increasing levels of Aβ40 may be sensitive indicators of conversion to AD, possibly reflecting compartmentalization of Aβ peptides in the brain. 3 key findings →
Participants: 225 Evidence: moderate
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Neurodegenerative tauopathies characterized by hyperphosphorylated tau include frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Mutations in the gene encoding TDP-43-the major protein component of neuronal aggregates characteristic of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitin-positive inclusion bodies-have been linked to familial forms of both disorders. 2 key findings →
Evidence: low
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) beginning in October 2004, is a 6-year research project that studies changes of cognition, function, brain structure and function, and biomarkers in elderly controls, subjects with mild cognitive impairment, and subjects with Alzheimer's disease (AD). 2 key findings →
Evidence: low
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These plasma ceramides may be early indicators of AD progression. 3 key findings →
Design: cross-sectional Participants: 25 Evidence: low
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Obesity is associated with lower brain volumes in cognitively normal elderly subjects, but no study has yet investigated the effects of obesity on brain structure in patients with mild cognitive impairment (MCI) or Alzheimer's disease (AD). 4 key findings →
Participants: 399 Evidence: low
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The number of people with dementia has increased dramatically with global ageing. 4 key findings →
Participants: 1,462 Evidence: low
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About hundred years ago, Oskar Fischer proposed that the senile plaques are the consequence of the deposition of a foreign substance that could induce an inflammatory response leading to an abnormal neuritic response of the surrounding neurons. 4 key findings →
Design: cohort study Evidence: moderate
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Systemic infection and drugs with anticholinergic effects are well-recognised and prevalent risk factors for delirium in elderly people. 4 key findings →
Evidence: low
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The text describes cerebral small vessel disease as a group of pathological processes affecting the brain's small vessels, with age-related and hypertension-related forms and cerebral amyloid angiopathy being most common. 3 key findings →
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No statistically significant improvement in the primary outcome measures (MMSE and ADAS-Cog) was observed with drug therapy at 36 weeks, at which point all groups had lost, on average, 1 point on the MMSE and gained 2-3 points on the ADAS-Cog scale compared with baseline. 5 key findings →
Participants: 938 Evidence: high
Full summary, score breakdown and related studies → Original source
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
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.
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 27,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →