27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Oral treatment of the amyloid prone AD-like APPPS1 mice with spermidine reduced neurotoxic soluble Aβ and decreased AD-associated neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CUMS induced depressive-like behaviors and cognitive decline in mice, which could be reversed by inhibiting NLRP3 inflammasome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Administration of DSS induced colitis, impaired spatial and recognition memory, activated microglia, and increased A1-like astrocyte numbers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that brain YKL-40 immunoreactivity was observed in a subset of astrocytes in all four diseases and in controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Roles for excitotoxicity and inflammation in Alzheimer's disease have been hypothesized. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
The memory-enhancing effect of IVIg reported here suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD. 3 key findings →
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
The data support that the midbrain may be more sensitive to the neuroinflammatory effects of subchronic air pollution exposure. 4 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 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
Alzheimer's disease (AD) is an age-related disorder characterized by progressive cognitive decline and dementia. 3 key findings →
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
Obesity is associated with numerous adverse neural effects, including reduced neurogenesis, cognitive impairment, and increased risks for developing Alzheimer's disease (AD) and vascular dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Across diverse viral infections, strong convergence was observed in innate immune activation pathways, including microglial priming and NLRP3 inflammasome signaling, accompanied by chronic production of proinflammatory cytokines (IL-1β, TNF-α, IFN-γ). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here we showed that activation of primary astrocytes from TR APOE mice with LPS led to TR APOE-dependent differences in cytokine secretion that were greatest in TR APOE2 and that were associated with differences in NF-kappaB subunit activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We show that inhibition of γ-secretase-dependent cleavage of the TREM2 C-terminal fragment in cellular membranes interferes with TREM2-dependent signaling and cellular function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified four SNPs (rs335929, rs335930, rs335931 and rs455671) were significantly associated with CSVD presence. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
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. 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 →