41/100
Neurodegeneration is a debilitating condition that causes nerve cell degeneration or death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Previous studies proposed the Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a receptor expressed in myeloid cells including microglia in brain and osteoclasts in bone, as a link between brain and bone disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane receptor on myeloid cells and plays an important role in the body's immune defense. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TREM2 (Triggering receptor expressed on myeloid cells 2) is the causative gene for Nasu-Hakola disease, which is characterized by multiple bone cysts and leukoencephalopathy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells-2 (TREM2) and colony-stimulating factor 1 receptor (CSF1R) are crucial molecules for microgliopathy, which is characterized by microglia dysfunction and has recently been proposed as the neuropathological hallmark of neurological disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2) increases the risk of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Consistent with previous in vitro findings, Trem2 H157Y increases TREM2 shedding with elevated soluble TREM2 levels in the brain and serum. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report an effective surface immobilization protocol for capture of Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a receptor whose elevated concentration in cerebrospinal fluid has recently been associated with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common form of dementia, accounting for as much as three-quarters of cases globally with individuals in low- and middle-income countries being worst affected. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in a microglia-associated gene TREM2 increase the risk of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease is the most common form of dementia; its key pathological findings include the deposition of extracellular-neurotoxic-plaques composed of amyloid-beta (Ab). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Four out of 10 TREM2 mutant variants have been identified in the analyzed groups, namely rs75932628 C > T (R47H), rs142232675 C > T (D87N), rs143332484 C > T (R62H), and rs2234253 G > T (T96K). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Loss-of-function variants of triggering receptor expressed on myeloid cells 2 (TREM2) increase the risk of developing Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2), a pattern recognition receptor abundantly expressed on microglia, has been identified as one of the risk factors for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapses are bridges for information transmission in the central nervous system (CNS), and synaptic plasticity is fundamental for the normal function of synapses, contributing substantially to learning and memory. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Here, we demonstrated for the first time that CD3-CD122+NK1.1+ precursor NK (pNK) cells expressed TREM2 and their population increased in TREM2-overexpressing transgenic (TREM2-TG) mice compared with that in female C57BL/6 J wild type (WT) mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterized by an increasing deterioration of memory, which is concomitant with additional cognitive deficits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previously, we reported that H157Y, a rare coding variant on exon 3 of the triggering receptor expressed on myeloid cells 2 gene (TREM2), was associated with Alzheimer's disease (AD) risk in a Han Chinese population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current hypothesis of Alzheimer's disease (AD) postulates that amyloid β (Aβ) deposition in the brain causes tau inclusion in neurons and leads to cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is ranked as the third-most expensive illness and sixth leading cause of mortality. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The central role of the resident innate immune cells of the brain (microglia) in neurodegeneration has become clear over the past few years largely through genome-wide association studies (GWAS), and has rapidly become an active area of research. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cancer continues to be a substantial health concern and a leading cause of death in the United States and around the world. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor expressed on myeloid-derived cell types. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rare coding variants of the microglial triggering receptor expressed on myeloid cells 2 (TREM2) confer an increased risk for Alzheimer's disease (AD) characterized by the progressive accumulation of aggregated forms of amyloid β peptides (Aβ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transgenic animals displayed higher total exposure, calculated as the AUC based on SUV determined at 24h, 48h, and 72h post injection, of PET radioligand [124I]mAb1729-scFv8D3CL than WT mice. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Obstructive Sleep Apnea and Cognitive Decline: A Review of Potential Vulnerability and Protective Factors
- Activated microglia mitigate Aβ-associated tau seeding and spreading
- Endocannabinoid System Genes in Dementia: A Systematic Mendelian Randomization Study of Functional Variants and Tissue-Specific Expression Across Clinical, Molecular, and Neuroimaging Phenotypes
- Clinical, genetic, and neuropathologic characteristics of posterior cortical atrophy
- Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier
- The UK Biobank resource with deep phenotyping and genomic data
- Optineurin deficiency disrupts phosphorylated tau proteostasis and clusterin expression in human neurons
- Influence of Cardiometabolic and Alzheimer Disease Genetics on Cognitive-Related Outcomes in a Diverse Population
- Decreased lipidated ApoE-receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes
- GWAS of longitudinal amyloid accumulation on18F-florbetapir PET in Alzheimer’s disease implicates microglial activation geneIL1RAP
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →