30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Although recent clinical trials targeting amyloid-β in Alzheimer's disease have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with amyloid-β metabolism and amyloid pathology might be important to halt the clinical deterioration. 4 key findings →
Design: longitudinal study Participants: 75 Evidence: moderate
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Understanding the exact pathophysiological mechanisms underlying the involvement of triggering receptor expressed on myeloid cells 2 (TREM2) related microglia activation is crucial for the development of clinical trials targeting microglia activation at different stages of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Participants: 1,001 Evidence: moderate
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. 4 key findings →
Design: cross-sectional Participants: 1,027 Evidence: moderate
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by amyloid-beta (Aβ) accumulation and neuroinflammation. 4 key findings →
Design: clinical trial Participants: 21 Evidence: high
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Alzheimer's disease (AD) is heterogenous at the molecular level. 4 key findings →
Participants: 419 Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disease with a complex and heterogeneous pathophysiology. 4 key findings →
Evidence: low
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Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up. 3 key findings →
Design: longitudinal study Evidence: moderate
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TREM2 is an innate immune receptor expressed on the surface of microglia. 4 key findings →
Design: cross-sectional Evidence: low
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The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. 4 key findings →
Participants: 37 Evidence: moderate
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Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Participants: 3,350 Evidence: low
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Neuro-inflammation was not reduced between the neflamapimod and placebo groups, and no change was observed in [18F]-DPA-714 PET. 5 key findings →
Design: randomized controlled trial Participants: 17 Evidence: high
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Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking. 4 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
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CSF sTREM2 levels are positively associated with an increased risk of AD and MCI. 5 key findings →
Design: systematic review Evidence: high
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Reliable noninvasive biomarkers are an unmet clinical need for the diagnosis of NASH. 4 key findings →
Design: cross-sectional Participants: 48 Evidence: moderate
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Short-term memory dysfunction is a key early feature of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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Neuroinflammation has gained increasing attention as a potential contributing factor in Alzheimer's disease (AD) pathology. 4 key findings →
Participants: 399 Evidence: moderate
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The NTK contains promising markers that improve the pathophysiological characterization of AD. 1 key finding →
Participants: 720 Evidence: low
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Microglial activation is a central player in the pathophysiology of Alzheimer's disease (AD). 2 key findings →
Participants: 101 Evidence: moderate
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The profile of many established and emerging CSF biomarkers of AD in a cohort of adults with DS was similar to that reported in LOAD and ADAD, while some differences were observed. 1 key finding →
Participants: 44 Evidence: moderate
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Neuroinflammation is associated with Alzheimer's disease, but the application of cerebrospinal fluid measures of inflammatory proteins may be limited by overlapping pathways and relationships between them. 2 key findings →
Participants: 382 Evidence: low
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Alzheimer's disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. 4 key findings →
Participants: 100 Evidence: moderate
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TREM2 was suggested to be an important regulator of microglia during neurodegeneration, but previous studies report conflicting results in relation to soluble TREM2 (sTREM2) in cerebrospinal fluid (CSF) when using clinical criteria to classify Alzheimer's disease (AD). 4 key findings →
Participants: 497 Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM-2) is a membrane-bound receptor expressed by microglia and macrophages.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor expressed by microglia. 3 key findings →
Participants: 299 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. 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →