31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Previous studies have demonstrated resilience to AD-related neuropathology in a form of cognitive reserve (CR). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Educational attainment is widely accepted as a cognitive reserve variable. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We tested if cognitive and brain reserve and maintenance explain individual differences in episodic memory and other cognitive domains from late middle to early older adulthood. 3 key findings →
Participants: 1,604 Evidence: low
Full summary, score breakdown and related studies → Original source
The gender-specific results for obesity, but not for diabetes, suggests that the underlying mechanisms linking them to cognition may be different. 2 key findings →
Participants: 551 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Late-life depression (LLD) increases risk for dementia and brain pathology, but possibly this is only true for one or more symptom profiles of LLD. 1 key finding →
Participants: 4,354 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Astrocytic injury and endothelial activation are interconnected processes within the neurovascular system that may contribute to variability in cognitive performance among cognitively unimpaired adults. 3 key findings →
Design: cross-sectional Participants: 313 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This is the first demonstration of gender differences in brain ferritin iron levels. 4 key findings →
Evidence: low
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Mutations in the CHCHD10 gene have been recently identified in a large family with a complex phenotype variably associating frontotemporal dementia (FTD) with amyotrophic lateral sclerosis (ALS), cerebellar ataxia, myopathy, and hearing impairment. 1 key finding →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep, EEG and mental function variables were studied in 44 subjects diagnosed as having probable senile dementia of the Alzheimer's type (SDAT) and 22 controls matched for age and minimal depression. 3 key findings →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cognitive reserve (CR) is defined as the ability to maintain functionality despite accumulating pathology. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Although poor sleep quality and extreme sleep durations have been associated with brain atrophy and dementia, it is unclear whether sleep disturbances contribute to neural injury in the absence of neurodegeneration and cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The study of factors, across species, that allow some individuals to age more successfully than others has important implications for individual wellbeing as well as health education, policy and intervention. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to explore the moderating effects of the frequently used cognitive reserve (CR) proxies [i.e., education, premorbid intelligence quotient (pIQ), occupational complexity (OC), and lifetime cognitive activity (LCA)] on the relationships between various in vivo Alzheimer's disease (AD) pathologies and cognition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitively stimulating environments are thought to be protective of cognitive decline and onset of Alzheimer's disease and related dementias (ADRD) through the development of cognitive reserve (CR). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Late-life depression (LLD) is associated with an increased risk of all-cause dementia and may involve Alzheimer's disease pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in fused in sarcoma (Fus) cause familial amyotrophic lateral sclerosis (ALS) and occasionally frontotemporal dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Level of education is often regarded as a proxy for cognitive reserve in older adults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain age prediction is a machine learning method that estimates an individual's chronological age from their neuroimaging scans. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traffic-related air pollution (TRAP) is associated with lower cognition and reduced white matter volume in older adults, specifically for particulate matter <2.5-μm diameter (PM 2.5 ). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ensuing homeostatic responses to myelin breakdown further increase intracortical toxicity and results in the relentless progression and non-random anatomical distribution of AD lesions that eventually cause neuronal dysfunction and degeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exposure to environmental toxins such as pesticides is implicated in increasing Alzheimer's disease risk. 2 key findings →
Evidence: low
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events