Simvastatin-related reductions in CSF p-tau 181 concentrations may be modulated by LDL cholesterol. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Simvastatin-related reductions in CSF p-tau 181 concentrations may be modulated by LDL cholesterol. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that higher glucose levels may be a risk factor for dementia, even among persons without diabetes. 4 key findings →
Participants: 839 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previously published community- or population-based studies of brain aging and dementia with autopsy were restricted to a single sex, a single ethnic group, Roman Catholic clergy, or focused pathological assessments. 2 key findings →
Design: longitudinal study Participants: 221 Evidence: moderate
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Employing time-dependent proportional hazards modeling, the authors found no significant association between statin use and incident dementia or probable AD. 2 key findings →
Design: cohort study Participants: 312 Evidence: moderate
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Statins may modulate the phosphorylation of tau in humans and this effect may depend on the CNS availability of the statin. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that search strategies that use automated electronic search strategies to extract Charlson comorbidities from the clinical notes contained within the electronic medical record are feasible and reliable. 3 key findings →
Design: cohort study Participants: 1,447 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Whether mild TBI (mTBI) in veterans confers a similar increased risk of AD is less known. 4 key findings →
Design: case-control study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, the effect sizes were small. 1 key finding →
Participants: 34 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The data do not support an association between serum total cholesterol or high density lipoprotein in late life and subsequent risk of dementia or Alzheimer disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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This study aims to systematically evaluate the efficacy of Pet robot intervention (PRI) for people with dementia. 4 key findings →
Design: systematic review Evidence: high
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In a single center, the ICD-9 code V66.7 had poor sensitivity and high specificity for identifying hospitalized patients who received a palliative care consultation. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most experts consider that memantine has a symptomatic treatment, but clinical trials have not yet provided compelling evidence to support a disease-modifying effect. 3 key findings →
Evidence: high
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This enlarged study confirms earlier findings that statin therapy in early old age, but not in late age, may be associated with a lower risk of AD. 4 key findings →
Participants: 3,099 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings demonstrate an association between antecedent statin use and neurofibrillary tangle burden at autopsy. 4 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The gut microbiota comprises a complex community of microorganism species that resides in our gastrointestinal ecosystem and whose alterations influence not only various gut disorders but also central nervous system disorders such as Alzheimer's disease (AD). 4 key findings →
Evidence: low
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These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition. 2 key findings →
Evidence: low
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Phosphorylation of tau protein is a critical event in the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Intracellular aggregation of the microtubule-associated protein tau into filamentous inclusions is a defining characteristic of Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by impairments of cognitive function as a result of synaptic deficits and neuronal loss, is associated with inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide 1 (GLP-1) is a growth factor. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The incretins glucagon-like peptide 1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP) are growth factors with neuroprotective properties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucose-dependent insulinotropic polypeptide (GIP) is a member of the incretin hormones and growth factors. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Basal ganglia iron serves as a stage-dependent mediator linking pTau217 to hippocampal neurodegeneration, with prodromal AD potentially indicating a particularly vulnerable stage for iron-targeted interventions and iron profiling for patient stratification. 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation. 1 key finding →
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 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 →