27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Nicotinamide riboside (NR) increases blood levels of NAD+, a cofactor central to energy metabolism, and improves brain function in some rodent models of neurodegeneration. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
In moderate stages of amnestic mild cognitive impairment, common cognitive tests provide better predictive accuracy than measures of whole brain, ventricular, entorhinal cortex, or hippocampal volumes for assessing progression to Alzheimer disease. 1 key finding →
Participants: 129 Evidence: high
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Patients with MCI converted to AD at an annual rate of 17.2%. 2 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The prevalence of pathologic AD markers was very common (46%) in a representative population sample of 70-year-olds. 3 key findings →
Design: cohort study Participants: 322 Evidence: moderate
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Diabetes is related to a higher risk of amnestic MCI in a population with a high prevalence of this disorder. 5 key findings →
Design: cohort study Participants: 1,772 Evidence: moderate
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Among the 1430 cognitively normal participants included, the mean (SD) age was 79.5 (5.3) years, 49.4% were men, the mean duration of education was 14.3 years, and 25.4% were APOE ε4 carriers. 5 key findings →
Design: longitudinal study Participants: 1,630 Evidence: moderate
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Progression from amnestic mild cognitive impairment to Alzheimer disease in this cohort was best determined by combining four common, easily administered, cognitive measures. 1 key finding →
Participants: 539 Evidence: moderate
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In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline. 1 key finding →
Design: cohort study Participants: 110 Evidence: moderate
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Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. 2 key findings →
Design: longitudinal study Evidence: moderate
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Early tau deposition was elevated in women compared with men in individuals on the Alzheimer disease trajectory. 5 key findings →
Design: cross-sectional Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a frequent problem encountered in advanced stages of Parkinson disease (PD). 5 key findings →
Design: longitudinal study Evidence: moderate
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In ADNI, Aβ-positive participants showed more decline than did Aβ-negative participants with regard to the ADCS-PACC score at 24 months (mean [SE] difference, -1.239 [0.522] [95% CI, -2.263 to -0.215]; P = .02). 4 key findings →
Evidence: low
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Estimates of AD disease duration become more accurate if age, sex, setting, APOE, and cerebrospinal fluid tau are taken into account. 2 key findings →
Participants: 3,268 Evidence: low
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High Aβ participants were more likely to be APOE ε4+ than low Aβ participants. 2 key findings →
Design: cohort study Evidence: moderate
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When proper normative values are used, only age and education, and not race or ethnicity, are associated with higher frequency of MCI. 4 key findings →
Design: cohort study Evidence: moderate
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Although the presence of abnormal levels of amyloid-β (Aβ) is associated with higher rates of progression to clinically classified mild cognitive impairment or dementia, little research has evaluated potentially modifiable moderators of Aβ-related cognitive decline, such as anxiety and depressive symptoms. 5 key findings →
Design: cohort study Participants: 333 Evidence: moderate
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Our study indicates that changes in PVS-related MRI parameters occur in MCI and AD, possibly due to impairment of the glymphatic system. 3 key findings →
Participants: 36 Evidence: low
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Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ~20%. 2 key findings →
Design: meta-analysis Participants: 42 Evidence: high
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The apolipoprotein E (APOE) gene is the best established genetic risk factor for Alzheimer's disease in later life, with the ε4 allele conferring higher risk. 5 key findings →
Design: cohort Participants: 9,496 Evidence: moderate
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Aβ deposition increases slowly from cognitive normality to moderate severity DAT. 5 key findings →
Participants: 206 Evidence: low
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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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If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly. 2 key findings →
Design: cross-sectional Participants: 54 Evidence: moderate
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This should be considered when designing protocols for amyloid-modifying clinical trials. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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 →