28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Principle component analyses identified 3 factors: trophic (BDNF, VEGF, TGFβ), degenerative (GFAP, NfL), and inflammatory (TNFα, IL-6, IP-10, IL-10). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by impairments of cognitive function as a result of synaptic deficits and neuronal loss, is associated with inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A hallmark of Alzheimer's disease (AD) is the aggregation of β-amyloid peptides (Aβ) into amyloid plaques in patient brain. 2 key findings →
Participants: 138 Evidence: low
Full summary, score breakdown and related studies → Original source
Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Subcortical small-vessel disease (SSVD) is a disorder well characterized from the clinical, imaging, and neuropathological viewpoints. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
App NL/NL and App NL-G-F/NL-G-F mice exhibit behavioral changes associated with non-cognitive, emotional domains before the onset of definitive cognitive deficits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human mini-brains (MB) are cerebral organoids that recapitulate in part the complexity of the human brain in a unique three-dimensional in vitro model, yielding discrete brain regions reminiscent of the cerebral cortex. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings identify CatD as the principal intracellular Aβ-degrading protease identified to date, one that regulates Aβ42/40 ratios via differential degradation of Aβ42 vs. Aβ40. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid pathology occurs early in Alzheimer's disease (AD), and has therefore been the focus of numerous studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results show that different isoforms of Aβ can be detected in the human retina and moreover support the growing number of studies indicating that AD-related pathological changes occurring in the brain could be reflected in the retina. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intramembrane proteolysis of transmembrane substrates by the presenilin-γ-secretase complex is preceded and regulated by shedding of the substrate's ectodomain by α- or β-secretase. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) represents a major healthcare burden with no effective treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings highlight sexual dimorphism in the behavior, neuropathology, and plasma proteins in tau P301S transgenic AD mice, indicating that the use of male P301S transgenic mice may be more suitable for assessing anti-phosphorylated tau therapeutic strategies for AD and related tauopathies, and the MIP-3α may be a new potential plasma biomarker. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-isolated BEVs have emerged as a novel player in the study of AD, with enormous potential as a diagnostic, evaluation of therapeutics, and treatment tool. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral deposition of the beta-amyloid peptide (A beta) is an invariant feature of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid beta protein precursor (beta APP). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation in brain of senile plaques containing beta-amyloid protein (A beta) is a defining feature of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with impaired clearance of β-amyloid (Aβ) from the brain, a process normally facilitated by apolipoprotein E (apoE). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
One of the major neuropathological findings in the brains of individuals with Alzheimer's disease (AD) is a loss of synaptic contacts in both the neocortex and hippocampus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gene expression profiles of more than 10,000 individual microglial cells isolated from cortex and hippocampus of male and female App NL-G-F mice over time demonstrate that progressive amyloid-β accumulation accelerates two main activated microglia states that are also present during normal aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E4 (apoE4), one of the three common isoforms of apoE, has been implicated in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gene ontology analyses coupled with bioinformatics approaches revealed drug targets and transcriptional regulators of microglial modules predicted to favorably modulate neuroinflammation in AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are resident immune cells in the central nervous system (CNS) that originate from myeloid progenitor cells in the embryonic yolk sac and are maintained independently of circulating monocytes throughout life. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 6,970 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.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →