Both diseases exhibit common genetic, epigenetic, biochemical and physiological characteristics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Both diseases exhibit common genetic, epigenetic, biochemical and physiological characteristics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Tauopathies are a group of neurodegenerative disorders, including Alzheimer's disease, frontotemporal dementia, and progressive supranuclear palsy, characterized by the pathological accumulation of tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
hONE-NPCs expressed proteins such as Ki67, Nestin, GFAP, and b-III Tubulin, which are associated with cellular proliferation and the neuronal progenitor lineage. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here we present the cases of two individuals with language and behavioral symptoms indicative of the early clinical manifestations of both Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease (AD) is the most common form of dementia, characterized by progressive cognitive decline, memory impairment, synaptic dysfunction, and neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Advanced Glycation End Products (AGEs) are reactive compounds formed through the non-enzymatic glycation of proteins, lipids, or nucleic acids due to exposure to reducing sugars. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease is the leading cause of dementia and represents a growing global health challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia encompasses a group of progressive neurodegenerative disorders marked by cognitive, behavioural, and functional decline, underpinned by complex neurobiological processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (PGRN) causes frontotemporal dementia (FTD), a devastating neurodegenerative disease with no effective treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early Ap accumulation is associated with distinct gut microbial signatures and reduced neuroactive metabolic potential, identifying targets for potential preclinical AD intervention. 3 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
Intranasal insulin has been investigated as a metabolic intervention in Alzheimer’s disease (AD), but its effects across the brain–gut axis remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Environmental exposures are major but understudied determinants of chronic disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is a progressive, currently irreversible, neurodegenerative disorder associated with the accumulation of β-Amyloid (Aβ) plaques between cells and tau (τ) tangles within cells. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized primarily by progressive cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases comprise a diverse group of progressive disorders characterized by the selective and irreversible loss of neuronal structure and function within the specific regions of the central and/or peripheral nervous systems. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
The Amaryllidaceae geophyte Lycoris radiata is a primary botanical source of high-value medicinal alkaloids, including the Alzheimer’s therapeutic galanthamine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Bee venom (BV) contains bioactive peptides with potent antioxidant, anti-inflammatory, and neuroprotective properties, yet its direct therapeutic use is limited by cytotoxicity, instability, and uncontrolled release. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings identify TTR as a contributor of adaptive neurovascular homeostasis during gut-derived neuroinflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder influenced by genetic, environmental, and lifestyle factors. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gut microbiome differences in Alzheimer’s disease (AD) are typically cataloged taxon by taxon, yet bacterial competition and cross-feeding make species’ roles dependent on the entire community. 1 key finding →
Participants: 274 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research on gut microbiota in Alzheimer’s disease (AD) has progressed from observational correlations to the validation of causal relationships. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings provide evidence that age-related changes in the gut microbiota, particularly reductions in Bifidobacterium , partially mediate cognitive decline in older adults. 5 key findings →
Design: cross-sectional Participants: 578 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β plaques, neurofibrillary tau tangles, neuroinflammation, and progressive cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →