29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →
Evidence: low
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The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →
Evidence: low
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M07-TFN showed higher binding affinities and stronger activation of hTREM2 signaling than all previously described anti-hTREM2 antibodies. p-Syk activation was increased 30-fold in hTREM2-overexpressing HEK293 cells and fourfold in human microglia cells compared to baseline. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most prevalent neurodegenerative disease associated with accumulation of amyloid beta peptides and intracellular neurofibrillary tangles formed by hyperphosphorylated Tau. 1 key finding →
Evidence: low
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Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component. 4 key findings →
Design: case-control study Participants: 98 Evidence: moderate
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This study replicated the associations of SORL1, CR1, ADAM17, RASGEF1C, SPI1 , and ADAMTS1 with AD risk and protection are found in Cuban Americans. 4 key findings →
Participants: 239 Evidence: low
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We aimed to investigate the potential therapeutic effects of the active substance of green tea, epigallocatechin-3-gallate (EGCG), on behavioral phenotypes and markers of neurogenesis in an Alzheimer disease (AD) rat model. 4 key findings →
Evidence: low
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HIV-associated neurocognitive disorders (HAND) affect 30%-50% of individuals living with HIV on combination antiretroviral therapy, with Alzheimer 's-like pathology as a potent comorbidity of HAND. 2 key findings →
Evidence: low
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Alzheimer's Disease (AD) is a progressive neurodegenerative disorder and the leading cause of cognitive decline in older adults. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
: ACTB: actin, beta; AD: Alzheimer disease; ADAM10: a disintegrin and metallopeptidase domain 10; ADGGA: acyl diacylglyceryl glucuronide; AHexSIS: acylhexosyl sitosterol; AHexSTS: acylhexosyl stigmasterol; AIF1/IBA1: allograft inflammatory factor 1; APP: amyloid beta precursor protein; ATG5: autophagy related 5; Aβ: amyloid β-protein; BACE1: beta-site APP cleaving enzyme 1; BASulfate: bile acid sulfate; BMP: bismonoacylglycerophosphate; CAR: acylcarnitine; CE: cholesteryl ester; Cer_NS: ceramide non-hydroxyfatty acid-sphingosine; CL: cardiolipin; CMA: chaperone-mediated autophagy; DAPI: 4',6-diamidino-2-phenylindole; DCAE: esterified deoxycholic acid; DEP: differentially expressed protein; DG: diacylglycerol; DGCC: diacylglyceryl-3-O-carboxyhydroxymethylcholine; DLG4/PSD95: discs large MAGUK scaffold protein 4; ECM: extracellular matrix; EtherLPC: ether-linked lysophosphatidylcholine; EtherLPE: ether-linked lysophosphatidylethanolamine; EtherMGDG: ether-linked monogalactosyldiacylglycerol; EtherOxPC: ether-linked oxidized phosphatidylcholine; EtherPC: ether-linked phosphatidylcholine; EtherPE: ether-linked phosphatidylethanolamine; EtherPG: ether-linked phosphatidylglycerol; EtherSMGDG: semino lipid; EtherTG: ether-linked triacylglycerol; FA: fatty acyls; FA: free fatty acid; FAHFA: fatty acid ester of hydroxyl fatty acid; FJC: fluoro-Jade C; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GDCAE: esterified glycodeoxycholic acid; GFAP: glial fibrillary acidic protein; GL: glycerolipids; GP: glycerophospholipids; HBMP: hemibismonoacylglycerophosphate; HexCer_NS: hexosylceramide non-hydroxyfatty acid-sphingosine; HSPA8/HSC70: heat shock protein 8; IP-MS: immunoprecipitation-mass spectrometry; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDGCC: lysodiacylglyceryl-3-O-carboxyhydroxymethylcholine; LDs: lipid droplets; LNAPE: N-acyl-lysophosphatidylethanolamine; LNAPS: N-acyl-lysophosphatidylserine; LPA: lysophosphatidic acid; LPC: lyso-phophatidylcholine; LPE: lysophosphatidylethanolamine; LPG: lysophosphatidylglycerol; LPI: lysophosphatidylinositol; LPS: lysophosphatidylserine; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MGDG: monogalactosyldiacylglycerol; MWM: Morris Water Maze; OA: oleic acid; OFT: Open Field Test; OxPC: oxidized phosphatidylcholine; OxPG: oxidized phosphatidylglycerol; OxPI: oxidized phosphatidylinositol; OxPS: oxidiz 1 key finding →
Evidence: low
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The obtained data is noteworthy. 4 key findings →
Design: case-control study Participants: 50 Evidence: moderate
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Altered β-amyloid (Aβ) homeostasis is a critical event triggering the shift from healthy aging to Alzheimer disease (AD) through the overproduction and impaired clearance of Aβ peptides. 2 key findings →
Evidence: low
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The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein. 2 key findings →
Evidence: low
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Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Bridging Integrator 1 (BIN1) is a genetic risk factor for late-onset Alzheimer disease. 2 key findings →
Evidence: low
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Intramembrane proteolysis by γ-secretase is critically implicated in Alzheimer disease pathogenesis by processing of its amyloid precursor protein substrate C99 into harmful amyloid-β peptide (Aβ) species. 2 key findings →
Evidence: low
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Alzheimer's disease (AD) stands as one of the primary neurological disorders affecting humans. 2 key findings →
Evidence: low
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Neuroinflammation plays a key role in Alzheimer's disease (AD), but the actions of microglial mediators may vary across stages of Aβ pathology. 1 key finding →
Evidence: low
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Most Alzheimer disease (AD) susceptibility genes have poorly understood roles in the central nervous system (CNS). 4 key findings →
Evidence: low
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MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation. 5 key findings →
Evidence: low
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The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
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The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Trans-active response DNA-binding protein-43 (TDP-43) is the major pathological protein in motor neuron disease and TDP-43 pathology has been described in the brains of up to 50% of patients with Alzheimer disease (AD). 5 key findings →
Evidence: low
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It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MDVs are small vesicles that bud from mitochondria and play an important role in removing damaged mitochondrial components. 5 key findings →
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →