We demonstrate that the small-molecule TREM2 ligand SULF A functions as an immunomodulator that reprograms microglia toward a reparative phenotype. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Microglia play a pivotal role in the pathology of Alzheimer's Disease (AD), with the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) central to their neuroprotective functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia performs a variety of functions during brain development designed to maintain brain homeostasis. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chronic neuroinflammation and impaired protein clearance are hallmarks of neurodegenerative diseases such as Alzheimer's disease (AD) and HIV-associated neurocognitive disorders (HAND). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
ITM2B/BRI2 mutations cause Alzheimer's Disease (AD)-related dementias. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TREM2, a microglia-specific receptor, is strongly associated with Alzheimer's disease (AD) risk, mediating microglial responses to amyloid pathology critical to AD development. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), represent significant global health challenges, affecting millions and straining healthcare systems. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane glycoprotein that plays a crucial role in the regulation of microglial survival, activation, phagocytosis, as well as in the maintenance of brain homeostasis and the inflammatory response to injury or neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results showed that IHT ameliorated cognitive function and Aβ pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Microglia, as resident macrophages in the central nervous system, play a multifunctional role in the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) is an incurable group of early-onset dementias that can be caused by the deposition of hyperphosphorylated tau in patient brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab, an anti-amyloid immunotherapy for Alzheimer's disease, efficiently reduces Aβ, though its plaque clearance mechanisms, long-term effects, and effects of discontinuation are not fully understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Alzheimer's disease (AD) and age-related macular degeneration (AMD) represent the leading causes of dementia and vision impairment in the elderly, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation plays an important role in the pathogenesis of various central nervous system (CNS) diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic periodontitis and its keystone pathogen, Porphyromonas gingivalis, have increasingly been linked with Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified a significant upregulation of COX-1 in 5 × FAD mice, with expression specifically localized to microglia in an age-dependent manner. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results demonstrate CA effectively inhibits NLRP3 inflammasome activation, reduces microglial pyroptosis, and mitigates oxidative stress-induced mitochondrial impairment in BV-2 cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
In vitro, PCSK9 significantly increased IL6, IL1B and TNFΑ mRNA levels in Aβ fibrils-treated U373 cells, without influencing inflammasome gene expression, except for an increase in NLRC4 mRNA levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the MWM, syringin reduced escape latency. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological role of interferon signaling is emerging in neuroinflammatory disorders, yet, the specific role of Interferon Regulatory Factor 3 (IRF3) in neuroinflammation remains poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a pervasive neurodegenerative disease that is estimated to represent approximately 70% of dementia cases worldwide, and the molecular complexity that has been highlighted remains poorly understood. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Neuroinflammation plays a vital role in determining the trajectory of Alzheimer's disease (AD) progression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a typical neurodegenerative disease, with the most highlighted pathologic changes identified in the β-amyloid peptide (Aβ) and neurofibrillary tangles (NFTs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 747 studies in this tag that have a study page, 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.
- Janus-faced microglia: beneficial and detrimental consequences of microglial phagocytosis
- The NALP3 inflammasome is involved in the innate immune response to amyloid-beta
- Sustained hippocampal IL-1beta overexpression impairs contextual and spatial memory in transgenic mice
- Sleep deprivation exacerbates microglial reactivity and Aβ deposition in a TREM2-dependent manner in mice
- DAP12 Stabilizes the C-terminal Fragment of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) and Protects against LPS-induced Pro-inflammatory Response
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System
- Effect of stress and peripheral immune activation on astrocyte activation in transgenic bioluminescent Gfap‐luc mice
- TREM2 and Neurodegenerative Disease
- Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease
- Meprin β cleaves TREM2 and controls its phagocytic activity on macrophages
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →