27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
< .01). All patient groups were also impaired on AVLT encoding, TMT-B and TMT B/A. Social and non-social neurocognitive functions differed between groups, with specific impairments in processing speed in VaD, emotion recognition in bv-FTD and memory retrieval in AD, and memory encoding and cognitive control impaired in all three groups. 4 key findings →
Evidence: low
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Oxidative stress is deeply involved in multiple pathological processes of VaD. 5 key findings →
Evidence: low
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Vascular dementia (VaD) is a neurodegenerative disorder characterized by chronic oxygen insufficiency, leading to the generation of oxygen-free radicals, inflammatory responses, disturbances in iron metabolism, lipid peroxidation, and other pathological changes that disrupt intracellular homeostasis. 5 key findings →
Evidence: low
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In this review, we outline the significant roles of necroptosis and its molecular mechanisms in the pathological process of VaD, with a particular focus on the role of necroptosis in modulating neuroinflammation and exacerbating the disruption of BBB permeability in VaD, and elaborate on the molecular regulatory mechanisms and the centrally involved cells of necroptosis mediated by tumor necrosis factor-α in neuroinflammation in VaD. 3 key findings →
Evidence: low
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Gait disturbances (odds ratio (OR) = 19.32; p = 0.01), visual-spatial complaints (OR = 6.06; p = 0.03), and visual hallucinations (OR = 31.06; p = 0.002) predicted DLB compared to AD, along with better memory (OR = 3.42; p = 0.003), naming (OR = 3.35; p = 0.002), and worse processing speed (OR = 0.51; p = 0.01). 5 key findings →
Evidence: low
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The spectral analysis of the resting-state eyes-closed electroencephalographic (rsEEG) activity typically shows abnormal delta (< 4 Hz), theta (4-7 Hz), and alpha (8-12 Hz) power in older patients with cognitive deficits due to progressive neurodegenerative diseases. 4 key findings →
Evidence: low
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: Integrating clinical bioinformatics with computational drug design, this study establishes a translational paradigm for nanomaterial development. 2 key findings →
Evidence: low
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We observed adults aged 50 years and older from the UK Biobank over a median observational period exceeding two years following COVID-19 infection. 5 key findings →
Evidence: low
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Tau aggregation driven by microtubule-associated protein tau (MAPT) mutations is central to frontotemporal dementia pathology, yet no disease-modifying therapies effectively target mutant tau. 4 key findings →
Evidence: low
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• To clarify the key role of Muscone delayed the development of vascular dementia (VD). • To reveal synaptic function in VD associated with neuronal pentraxin receptor (NP2). • To reveal that Muscone alleviates VD through the BDNF-TrkB-NP2 signaling pathway initially. 3 key findings →
Evidence: low
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Altered cerebrovascular hemodynamics and low cerebral perfusion contribute to the development and progression of dementia. 5 key findings →
Participants: 30 Evidence: low
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Participants across all groups showed significant differences in cognition and functionality. 5 key findings →
Participants: 141 Evidence: low
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Alzheimer's disease (AD) is one of the most common neurological disorders affecting older adults, with approximately 7.2 million cases only in the United States. 5 key findings →
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
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: 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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Both taus are very significantly correlated ( p 0,697 in all groups), and with YKL‐40 (r>0.430). 5 key findings →
Participants: 89 Evidence: low
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Cognitive impairment associated with Aβ positivity and low tau (A+T‐) is linked to mixed AD. 3 key findings →
Participants: 77 Evidence: low
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β =-0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
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The MoCA Solo is emerging as a reliable and efficient tool for assessing cognitive impairment in older adults. 3 key findings →
Participants: 40 Evidence: low
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Both V3 width and plasma Hcy concentration were negatively correlated with MoCA scores in PD (r=-0.358, P<0.001; r=-0.187, P=0.013, respectively). 5 key findings →
Evidence: low
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After 5 years, 666 (86.8%) individuals were followed up. 5 key findings →
Evidence: low
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LPA supported a three-profile solution: (1) lower depressive symptoms with moderate anxiety (33%), (2) severe combined depression and anxiety (18%) and (3) moderately severe depression with severe anxiety (49%). 5 key findings →
Design: cross-sectional Evidence: low
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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.
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 →