27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. 5 key findings →
Participants: 40 Evidence: low
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Overall, birth in an HSMS was associated with a 28% higher risk of dementia (adjusted hazard ratio [aHR], 1.28; 95% CI, 1.13-1.46) adjusted for age, sex, and race. 5 key findings →
Design: cohort study Participants: 7,423 Evidence: moderate
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Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. 4 key findings →
Evidence: low
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In addition to the deposition of β-amyloid plaques, neurofibrillary tangles composed of aggregated hyperphosphorylated tau are one of the pathological hallmarks of Alzheimer's disease and other neurodegenerative disorders. 1 key finding →
Design: systematic review Evidence: high
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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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Level of evidence Level V, systematic review. 3 key findings →
Design: systematic review Evidence: high
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The following 2 regions for tau burden were identified: the entorhinal cortex, which exhibits early signs of tauopathy, and the inferior temporal region, which is more closely associated with AD-related pathologic mechanisms. 4 key findings →
Design: cross-sectional Participants: 133 Evidence: low
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Previous neuroimaging studies reveal that MCI is associated with aberrant sensory-perceptual processing in cortical brain regions subserving auditory and language function. 5 key findings →
Evidence: low
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Both interventions were highly feasible and acceptable and allowed improvement in different aspects of cognitive and psychosocial functioning in MCI subjects. 4 key findings →
Evidence: high
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Each PPA clinical variant is associated with a typical and most frequent cognitive, neuroimaging, and neuropathological profile. 5 key findings →
Participants: 69 Evidence: moderate
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The purpose of this systematic review and meta-analysis was to evaluate the performance of cerebrospinal fluid (CSF) beta amyloid 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) as potential diagnostic biomarkers for idiopathic normal-pressure hydrocephalus (iNPH) and to assess their utility indistinguishing patients with iNPH from those with Alzheimer disease (AD) and healthy normal controls. 4 key findings →
Design: systematic review Participants: 413 Evidence: high
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Age-related cognitive impairment and dementia are an increasing societal burden. 4 key findings →
Evidence: low
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We thus examined whether higher blood cholesterol concentrations were associated with faster cognitive decline in a community-based longitudinal study of Chinese elderly. 4 key findings →
Design: longitudinal study Participants: 90 Evidence: moderate
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We observed 234 cases of all-cause dementia over 10 years of follow-up. 4 key findings →
Participants: 2,457 Evidence: low
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Sensitive detection of cognitive decline over the course of preclinical Alzheimer's disease is critical as the field moves toward secondary prevention trials. 4 key findings →
Design: longitudinal study Evidence: moderate
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Neuroinflammation in the form of microglial activation is present in synucleinopathies and is a potential therapeutic target to halt or delay the neurodegenerative process. 4 key findings →
Design: case-control study Participants: 20 Evidence: moderate
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According to study results, a higher adherence to the Mediterranean diet was associated with lower odds of frailty, irrespective of the definition used. 3 key findings →
Design: cross-sectional Participants: 1,740 Evidence: moderate
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A large number of non-pharmacological interventions for BPSD were identified. 2 key findings →
Evidence: low
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The associations with vascular dementia may be one component of a broader association between autoimmune diseases and vascular damage. 5 key findings →
Design: cohort study Participants: 827 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The combination of sAPPβ with YKL-40 and with NfL in CSF could be useful to increase the certainty of the diagnosis of FTLD-related syndromes in clinical practice. 2 key findings →
Design: cross-sectional Participants: 159 Evidence: moderate
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Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory. 1 key finding →
Design: cohort study Evidence: moderate
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At 6 mo, the n-3 FA group displayed marked increases in DHA and EPA plasma concentrations (2.6- and 3.5-fold), as well as decreased methylation in 2 out of 4 CpG sites ( P r = -0.25, P = 0.045; and r = -0.26, P = 0.041, respectively), but not to changes in plasma DHA concentration, and were not related to apolipoprotein E-4 allele frequency. 4 key findings →
Participants: 63 Evidence: high
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These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. 4 key findings →
Design: longitudinal study Evidence: moderate
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Mean age was 73.5 years and mean HbA1c was 6.8%. 3 key findings →
Design: cohort study 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 →