31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods. 3 key findings →
Participants: 165 Evidence: low
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This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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Cross-sectional functional magnetic resonance imaging studies using a memory task in patients with mild cognitive impairment have produced discordant results, with some studies reporting increased hippocampal activity--consistent with findings in genetic at-risk populations--and other studies reporting decreased hippocampal activity, relative to normal controls. 3 key findings →
Design: cross-sectional Participants: 33 Evidence: moderate
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Tensor-based morphometry can recover three-dimensional longitudinal brain changes over time by nonlinearly registering baseline to follow-up MRI scans of the same subject. 2 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
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Adjusted estimates of MTA were associated with significantly increased risk of developing dementia within 3 years, suggesting that obtaining a magnetic resonance image during the evaluation of MCI may offer additional independent information about the risk of progression to dementia. 2 key findings →
Participants: 190 Evidence: low
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Study objectives To determine the effect of self-reported clinical diagnosis of obstructive sleep apnea (OSA) on longitudinal changes in brain amyloid PET and CSF biomarkers (Aβ42, T-tau, and P-tau) in cognitively normal (NL), mild cognitive impairment (MCI), and Alzheimer's disease (AD) elderly. 2 key findings →
Design: longitudinal study Participants: 516 Evidence: moderate
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The vitamin E and donepezil trial for the treatment of amnestic mild cognitive impairment (MCI) was conducted at 69 centers in North America; 24 centers participated in an MRI sub study. 2 key findings →
Participants: 131 Evidence: low
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Disease modifying drugs for Alzheimer's disease (AD) are likely to be most effective when given in non-demented subjects. 4 key findings →
Design: meta-analysis Evidence: high
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It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI). 4 key findings →
Design: cohort study Participants: 185 Evidence: moderate
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From a longitudinal study of normal (Clinical Dementia Rating [CDR] = 0; n = 77) and mildly impaired (CDR = 0.5; n = 167) participants with 5 or more annual clinical assessments, baseline level of cognitive impairment in daily life was graded using CDR sum of boxes (CDR-SB) and level of cognitive performance impairment was graded using neuropsychological test scores. 4 key findings →
Design: longitudinal study Participants: 77 Evidence: moderate
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder with no cure, and available treatments are only able to postpone the progression of the disease. 4 key findings →
Design: systematic review Evidence: high
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A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed. 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
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Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI. 5 key findings →
Design: longitudinal study Participants: 186 Evidence: moderate
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The First Key Symposium was held in Stockholm, Sweden, 2-5 September 2003. 5 key findings →
Evidence: low
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In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
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Based on the title and abstracts, 830 papers were screened from which 250 primary research papers met the eligibility criteria (original research articles with patients or with a strict diabetes model without comorbidities, that included direct data about microglia in the brain or retina), and 17 additional research papers were included through forward and backward citations, resulting in a total of 267 primary research articles included in the scoping systematic review. 5 key findings →
Design: systematic review Participants: 267 Evidence: high
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Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
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Increasing cerebral Abeta deposition with age is the pathobiological phenotype of APOE4. 1 key finding →
Participants: 241 Evidence: low
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This should be considered when designing protocols for amyloid-modifying clinical trials. 1 key finding →
Design: longitudinal study Evidence: moderate
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These findings from healthy high-risk older individuals suggest that OI reflects degree of preclinical AD pathology, while its relationships with age and cognition result from the association of these latter variables with such pathology. 3 key findings →
Design: cross-sectional Participants: 101 Evidence: moderate
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Cognitively normal elderly individuals who engage in specific mentally stimulating activities even in late life have a decreased risk of incident MCI. 3 key findings →
Design: cohort study Participants: 973 Evidence: moderate
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No significant differences emerged in the probability of conversion from MCI to AD or dementia between the treated groups and the placebo groups. 5 key findings →
Evidence: high
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A history of hypertension is related to a higher risk of MCI. 5 key findings →
Design: cohort study Participants: 918 Evidence: moderate
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Recently, several animal studies indicated that the 'gut-brain' axis might contribute to the amyloid deposition of AD. 5 key findings →
Design: cross-sectional Participants: 97 Evidence: low
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Impaired memory and language were useful predictors of transition to AD. 2 key findings →
Participants: 2,364 Evidence: low
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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.
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