Docosahexaenoic acid (DHA), the main omega-3 fatty acid, is concentrated and avidly retained in membrane phospholipids of the nervous system. 1 key finding →
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.
Frozen brain specimens from patients with multiple sclerosis (MS) and other neurologic diseases were analyzed using immunocytochemical techniques for the presence of TNF. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The contribution of inflammation to the progression of neurodegenerative diseases such as Alzheimer's, Parkinson's, and prion diseases is poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple sclerosis (MS) brain tissue, spleen, and PBMC were studied using immunocytochemistry and FACS for immunoreactivity for lymphotoxin (LT) and TNF. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reactive microglia associated with the beta-amyloid plaques in Alzheimer's disease (AD) brains initiate a sequence of inflammatory events integral to the disease process. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are immune system cells associated with Alzheimer's disease plaques containing beta-amyloid (A beta). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are resident immune cells of the CNS that are activated by infection, neuronal injury, and inflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The endocannabinoid system is still poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial activation is central to the inflammatory response in Alzheimer's Disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence supports a role of neuroinflammation in the pathogenesis of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Microglia are the brain's tissue macrophages and are found in an activated state surrounding beta-amyloid plaques in the Alzheimer's disease brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The accumulation of aggregated amyloid β (Aβ) peptides in the brain is deeply involved in Alzheimer disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There are currently no effective therapeutics for Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent laboratory and gene sequencing data suggest that variations in receptors called the "triggering-receptors-expressed-on-myeloid-cells" (TREMs) are implicated in Alzheimer's disease, Parkinson's disease, multiple sclerosis, and frontotemporal lobar degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a common neurodegenerative disorder, strongly related with age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that changes in the triggering receptor expressed on myeloid cells 2 (TREM2) is closely correlated with the pathological development of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, which has been currently considered as a genetically complex disorder caused by a combination of environmental and genetic risk factors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Neuroinflammation plays a prominent role in the pathogenesis of vascular dementia (VD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The triggering receptor expressed on myeloid cells 2 (TREM2) is a multifunctional surface protein that affects survival, migration, and phagocytic capacity of myeloid cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previously, we showed that overexpression of triggering receptor expressed on myeloid cells 2 (TREM2), a microglia-specific immune receptor, in the brain of a middle-aged (7 months old) APPswe/PS1dE9 mice could ameliorate Alzheimer's disease (AD)-related neuropathology by enhancement of microglial amyloid-β (Aβ) phagocytosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In late-onset Alzheimer disease (AD) pathogenesis, genes, infections and immunity could be significant factors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia characterized by the deposition of extracellular amyloid-β (Aβ)-containing plaques, the formation of intraneuronal neurofibrillary tangles as well as neuroinflammatory changes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 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 10. The same 10 appear here every time.
- Pathological Roles of INPP5D in Alzheimer's Disease
- Potential Repositioning of Anti-cancer EGFR Inhibitors in Alzheimer's Disease: Current Perspectives and Challenging Prospects
- GWAS of longitudinal amyloid accumulation on18F-florbetapir PET in Alzheimer’s disease implicates microglial activation geneIL1RAP
- Targeting MicroRNA-485-3p Blocks Alzheimer's Disease Progression
- Role of trigger receptor 2 expressed on myeloid cells in neuroinflammation－neglected multidimensional regulation of microglia
- Mechanistic study of PHLDA1 in cognitive dysfunction of Alzheimer’s disease model mice via FoxO1‑mediated neuroinflammation
- TLR4 Cross-Talk With NLRP3 Inflammasome and Complement Signaling Pathways in Alzheimer's Disease
- The blood-brain barrier in systemic inflammation
- Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons
- Iron accumulation in microglia triggers a cascade of events that leads to altered metabolism and compromised function in APP/PS1 mice
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 →