Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These data suggest a revision of the original ADAPT hypothesis that NSAIDs reduce AD risk, as follows: NSAIDs have an adverse effect in later stages of AD pathogenesis, whereas asymptomatic individuals treated with conventional NSAIDs such as naproxen experience reduced AD incidence, but only after 2 to 3 years. 5 key findings →
Participants: 54 Evidence: high
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After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P Conclusions and relevance We provide robust evidence of a stronger association between APOE-ε4 and CSF tau levels among women compared with men across multiple independent data sets. 5 key findings →
Design: cohort study Participants: 1,798 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The lack of strong association between brain beta-amyloid deposition and cognitive impairment has been a challenge for the Alzheimer's disease (AD) field. 4 key findings →
Design: meta-analysis Participants: 678 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Neuropathology was ubiquitous, with 94% of participants having 1+, 78% having 2+, 58% having 3+, and 35% having 4+. 1 key finding →
Design: longitudinal study Participants: 1,079 Evidence: moderate
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Pooled clinical and neuropathologic data from 3 prospective cohort studies indicate that TBI with LOC is associated with risk for Lewy body accumulation, progression of parkinsonism, and PD, but not dementia, AD, neuritic plaques, or neurofibrillary tangles. 5 key findings →
Design: cohort study Participants: 7,130 Evidence: moderate
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We tested the hypothesis that cerebral amyloid angiopathy (CAA) is related to Alzheimer disease (AD) dementia and decline in multiple cognitive systems in old age, independent of AD plaque and tangle pathology and other common age-related neuropathologies. 4 key findings →
Design: longitudinal study Participants: 1,113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's dementia is significantly more common in women than in men. 4 key findings →
Design: longitudinal study Participants: 971 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →
Design: cohort study Participants: 4,467 Evidence: moderate
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Alzheimer's disease is the leading cause of dementia worldwide, but the cellular pathways that underlie its pathological progression across brain regions remain poorly understood 1-3 . 4 key findings →
Participants: 48 Evidence: low
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Brain DNA methylation in multiple AD loci is associated with AD pathologies. 5 key findings →
Design: cohort study Participants: 447 Evidence: moderate
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Subjects were 404 persons in the Religious Orders Study, a cohort study of aging, who underwent annual clinical evaluations, including 19 neuropsychological tests from which 5 cognitive domain and global summary scores were derived, and brain autopsy at time-of-death (mean age-at-death 86). 4 key findings →
Design: cohort study Participants: 404 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulating data suggest that cerebrovascular disease contributes to Alzheimer's disease pathophysiology and progression toward dementia. 5 key findings →
Design: cohort study Participants: 1,722 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal clinical-pathological studies have increasingly recognized the importance of mixed pathologies (the coexistence of one or more neurodegenerative and cerebrovascular disease pathologies) as important factors in the development of Alzheimer's disease (AD) and other forms of dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. 1 key finding →
Participants: 515 Evidence: low
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Glia have been implicated in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
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The pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older persons with and without dementia, but the extent to which they account for late life cognitive decline remains unknown. 4 key findings →
Design: longitudinal study Participants: 856 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02). 5 key findings →
Design: cohort study Participants: 286 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The results suggest that the contribution of education to cognitive reserve is limited to its association with level of cognitive function before old age. 4 key findings →
Design: cohort study Participants: 2,899 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood. 3 key findings →
Participants: 427 Evidence: low
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Better sleep consolidation attenuates the effect of APOE genotype on incident AD and development of neurofibrillary tangle pathology. 2 key findings →
Design: cohort study Participants: 698 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline is a leading cause of disability and death in old age but its neurobiological bases are not well understood. 4 key findings →
Design: cohort study Participants: 130 Evidence: moderate
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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