Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer's disease (AD) and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Atherosclerotic lesions are known for their cellular heterogeneity, yet the molecular complexity within the cells of human plaques has not been fully assessed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic studies have highlighted microglia as pivotal in orchestrating Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuronal circuit assembly requires the fine balance between synapse formation and elimination. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tissue-resident and recruited macrophages contribute to both host defense and pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Brain macrophage populations include parenchymal microglia, border-associated macrophages, and recruited monocyte-derived cells; together, they control brain development and homeostasis but are also implicated in aging pathogenesis and neurodegeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The role of microglia in the amyloid cascade of Alzheimer's disease (AD) is debated due to conflicting findings. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls. 3 key findings →
Design: meta-analysis Participants: 23,092 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We review the genetic risk factors for late-onset Alzheimer's disease (AD) and their role in AD pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to increased Alzheimer's disease (AD) risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Haplodeficiency of the microglia gene TREM2 increases risk for late-onset Alzheimer's disease (AD) but the mechanisms remain uncertain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor genetically linked to the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia and complement can mediate neurodegeneration in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are crucial for maintaining brain health and neuron function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A causative association was recently demonstrated between homozygous TREM2 mutations and frontotemporal dementia (FTD)-like syndrome and between heterozygous TREM2 exon2 genetic variations and late-onset Alzheimer's disease (AD). 4 key findings →
Participants: 1,030 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Although mutations within the TREM2 gene have been robustly associated with Alzheimer's disease, it is not known whether alterations in the regulation of this gene are also involved in pathogenesis. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression. 4 key findings →
Design: cross-sectional Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking. 4 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CSF sTREM2 levels are positively associated with an increased risk of AD and MCI. 5 key findings →
Design: systematic review Evidence: high
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.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →