28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline and functional impairment, primarily driven by the accumulation of amyloid-beta (Aβ) plaques and tau tangles. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and vascular dementia (VaD) are the two commonest causes of dementia in older adults and frequently coexist as mixed neurodegenerative-cerebrovascular pathology. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chlamydia pneumoniae is an intracellular bacterium implicated in Alzheimer's disease (AD), but its role in retinal pathology and disease progression is unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is marked by amyloid-β (Aβ) accumulation, tau pathology, and neuroinflammation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Peripheral immune cell infiltration and crosstalk with brain-resident cells critically drive Alzheimer's disease (AD)-associated neuroinflammation, highlighting its therapeutic potential. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), is a chronic age-related progressive neurodegenerative disorder, characterized by neuroinflammation and extracellular aggregation of Aβ peptide. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
There is increasing interest in studying retinal biomarkers for various neurodegenerative diseases. 2 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the leading cause of dementia, is characterized by early synaptic dysfunction that precedes overt cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive decline is closely associated with biological aging and with interconnected processes, including chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and cellular senescence. 2 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source
Neuropathological studies have shown that the typical neurofibrillary pathology of hyperphosphorylated tau protein in Alzheimer’s disease (AD) preferentially affects specific brain regions whereas others remain relatively spared. 5 key findings →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source
We have defined a new paraneoplastic immunoglobulin G (IgG) autoantibody specific for CRMP-5, a previously unknown 62-kd neuronal cytoplasmic protein of the collapsin response-mediator family. 2 key findings →
Participants: 121 Evidence: low
Full summary, score breakdown and related studies → Original source
Tau pathology is a hallmark of several neurodegenerative diseases, including frontotemporal dementia and Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The National Institute on Aging and the Alzheimer's Association convened three separate work groups in 2011 and single work groups in 2012 and 2018 to create recommendations for the diagnosis and characterization of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of epilepsy is increased among Alzheimer's Disease (AD) patients and cognitive impairment is common among people with epilepsy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We underline the potential of next-generation biomarker identification tools to detect novel proteomic features that also incorporate established biomarkers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the community, the concentration of AD blood biomarkers varies in relation to medical conditions and systemic inflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oligomeric-Aβ mediates the maturation of tau pathology and its neuronal toxicity in macaques but not its initial spreading. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This ITR analysis provides a proof of concept for precision medicine in future AD research and drug development. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings provide evidence that greater concentrations of KP metabolites are associated longitudinally over two years with greater biomarker evidence of neurofibrillary tau pathology (pTau-181), neuroinflammation (GFAP), and neurodegeneration (NfL), suggesting that dysregulated KP metabolism may play a role in ADRD pathogenesis. 4 key findings →
Participants: 301 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic loss strongly correlates with cognitive impairment in Alzheimer's disease (AD), yet the mechanism linking its origin and pattern remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive irreversible neurodegenerative disorder that represents a major global public health concern. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicate that neuroinflammation is linked to the symptomatic phase of ALS/FTD and shows a similar pattern in sporadic and genetic cases. 3 key findings →
Participants: 16 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The role of sAPP isoforms in iNPH seems to be independent from the amyloid cascade. 2 key findings →
Participants: 102 Evidence: low
Full summary, score breakdown and related studies → Original source
The combination of the CSF biomarkers T-tau, Aβ40 and MCP-1 separates iNPH from cognitive and movement disorders with good diagnostic sensitivity and specificity. 1 key finding →
Participants: 82 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 →