27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma biomarkers of AD neuropathology, neuronal injury, and astrogliosis increase with age and are associated with known dementia risk factors. 5 key findings →
Design: cohort Participants: 1,525 Evidence: high
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The included studies (n=15) assessed change in cognition in response to a multidomain lifestyle intervention. 5 key findings →
Design: systematic review Participants: 15 Evidence: high
Full summary, score breakdown and related studies → Original source
Our study confirmed the effectiveness of psychosocial interventions for improving cognition or slowing down the progression of cognitive impairment in AD patients and recommended several interventions for clinical practice. 3 key findings →
Design: meta-analysis Participants: 682 Evidence: high
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD) is recognized to be in the Alzheimer disease (AD) cognitive continuum. 4 key findings →
Design: cohort study Participants: 3,585 Evidence: moderate
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Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 350 Evidence: low
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After adjusting for various risk factors, participants with low socioeconomic status (vs high) had increased risk for early-onset dementia (3·38, 2·61-4·37), and overall lifestyle mediated 3·2% (1·8-5·7) of the association. 4 key findings →
Design: cohort study Participants: 345 Evidence: moderate
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Advanced glycation end products (AGEs) and their receptor (RAGE) are implicated in the pathophysiological processes of dementia and potentially underlie the association of diabetes with neurodegeneration. 4 key findings →
Design: cohort study Participants: 1,021 Evidence: moderate
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The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention. 4 key findings →
Participants: 4,110 Evidence: moderate
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Inflammatory protein biomarkers induced by immune responses have been associated with cognitive decline and the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Design: cross-sectional Participants: 708 Evidence: moderate
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In this large cohort of older adults, long-term PM2.5 exposure was associated with increased dementia incidence. 3 key findings →
Participants: 541 Evidence: moderate
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Long-term exposure to PM 2.5 , NO 2 , and/or BC in Denmark were associated with mortality beyond cardiorespiratory diseases, including diabetes, dementia, psychiatric disorders, asthma, and ALRI. 5 key findings →
Participants: 803,881 Evidence: moderate
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Plasma-based biomarkers would be potential biomarkers for early diagnosis of Alzheimer's disease (AD) because they are more available and cost-effective than cerebrospinal fluid (CSF) or neuroimaging. 4 key findings →
Design: cross-sectional Participants: 185 Evidence: moderate
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Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease. 2 key findings →
Participants: 77 Evidence: moderate
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Early diagnosis of Alzheimer's disease plays a pivotal role in patient care and clinical trials. 4 key findings →
Evidence: moderate
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Individuals with Alzheimer's disease (AD) dementia exhibit significant heterogeneity across clinical symptoms, atrophy patterns, and spatial distribution of Tau deposition. 4 key findings →
Design: longitudinal study Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein that is predominantly expressed by microglia in the brain. 4 key findings →
Evidence: low
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Infections have been associated with the incidence of Alzheimer disease and related dementias, but the mechanisms responsible for these associations remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins depends on contributions from surrounding glia. 4 key findings →
Evidence: low
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Overall, the CDT may be as effective as the MMSE or CASI as a first-level dementia screen for clinical use in multiethnic, multilingual samples of older adults. 3 key findings →
Participants: 295 Evidence: low
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Planning for the wide range of services necessary for care of those suffering from dementia should take into account ethnoracial differences in rates. 3 key findings →
Evidence: low
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Chimeric antigen receptor (CAR) -T cell therapy is an efficient therapeutic strategy for specific hematologic malignancies. 4 key findings →
Evidence: low
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The human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotactic activity of a variety of polypeptides associated with inflammation and bacterial infection, including the 42-amino acid form of amyloid beta peptide (Abeta42), a pathogenic factor in Alzheimer disease. 4 key findings →
Evidence: low
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Recent theories have suggested that chronic pain could be partly maintained by maladaptive physiological responses of the organism facing a recurrent stressor. 5 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
The results project substantial cost savings from implementing a blood test for AD pathology within the diagnostic pathway based on modeling results, which future research should confirm with actual data. 4 key findings →
Design: modelling Evidence: preliminary
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Disordered lipid accumulation in the arterial wall is a hallmark of atherosclerosis. 4 key findings →
Evidence: low
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 →