PLCG2 expression is restricted primarily to microglia and granule cells of the dentate gyrus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
PLCG2 expression is restricted primarily to microglia and granule cells of the dentate gyrus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alogliptin treatment alleviated LPS-induced cognitive impairment as assessed by Morris water maze and novel object recognition tests. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is the first demonstration of TLR4-dependent upregulation of cytokines in an AD mouse model. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Aβ clearance. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twelve months after infection, a time equivalent to middle to early elderly ages, mice had behavioral and neurological deficits, and brain MRIs showed mild to moderate ventricular dilatation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is growing evidence that excessive microglial phagocytosis of neurons and synapses contributes to multiple brain pathologies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several attempts have been made to treat Alzheimer's disease (AD) using anti-amyloid strategies with disappointing results. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adult neurogenesis occurs mainly in the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The NLRP3 inflammasome is a cytosolic multiprotein complex composed of the innate immune receptor protein NLRP3, adapter protein ASC, and inflammatory protease caspase-1 that responds to microbial infection, endogenous danger signals, and environmental stimuli. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Particulate ligands, including cholesterol crystals and amyloid fibrils, induce production of interleukin 1β (IL-1β) dependent on the cytoplasmic sensor NLRP3 in atherosclerosis, Alzheimer's disease and diabetes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with chronic inflammation are often associated with the emergence of depression symptoms, while diagnosed depressed patients show increased levels of circulating cytokines. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of the inflammasome, a macromolecular complex sensing cell stress or danger signals and initiating inflammation, was first introduced approximately a decade ago. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pro-inflammatory activation of microglia is a hallmark of Alzheimer's disease (AD), and this process involves a switch from oxidative phosphorylation (OXPHOS) toward glycolysis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of tumor necrosis factor (TNF) as an immune mediator has long been appreciated but its function in the brain is still unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder to date. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In addition to amyloid-β plaque and tau neurofibrillary tangle deposition, neuroinflammation is considered a key feature of Alzheimer's disease pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are the resident brain macrophages and they have been traditionally studied as orchestrators of the brain inflammatory response during infections and disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traditionally, lymphocytic interferon γ (IFN-γ) was considered to be a simple 'booster' of proinflammatory responses by microglia (brain-resident macrophages) during bacterial or viral infection. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are critical in brain development and Alzheimer's disease (AD) etiology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The excitotoxin quinolinic acid (QUIN) is synthesized through the kynurenine pathway (KP) by activated monocyte lineage cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
8 of the 384 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 8. The same 8 appear here every time.
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 →