27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer’s disease (AD) is characterized by progressive memory decline, with the medial entorhinal cortex (MEC) representing an early vulnerable hub for spatial cognition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Soluble amyloid-β (Aβ) oligomers are considered the primary neurotoxic species in Alzheimer’s disease, yet the relationship between oligomer structure and biological activity remains poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) staging based on amyloid-β, tau, and neurodegeneration does not capture heterogeneous microglial functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We define an astrocyte–microglia axis in which astrocytic sEH limits EET availability and thereby sustains microglial STING signaling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
ORIGIN-PD enables rational enrichment for NLRP3/NF-κB inhibitor trials by identifying patients with inflammatory involvement. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, pathological tau aggregation, and neuronal loss. 1 key finding →
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
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
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
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
This review examines nanocrystal-based theranostic platforms as a promising method to overcome the blood-brain barrier (BBB) in neurodegenerative diseases like Alzheimer’s and Parkinson’s. These neurological diseases involve gradual protein misfolding and aggregation, causing neuronal damage and loss. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular dysfunction is increasingly recognized as a feature of Alzheimer’s disease (AD), and inadequate oxygen delivery may contribute to neuronal death. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
FDA-approved carbonic anhydrase inhibitors (CAIs) have shown robust efficacy in reducing amyloid-β (Aβ) pathology, neurodegeneration, and cerebrovascular dysfunction in Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) models, highlighting carbonic anhydrase (CAs) as a promising, previously untapped therapeutic target for AD and vascular contribution to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Spermine exerts neuroprotective effects in VaD by inhibiting TRPM2-mediated oxidative stress and activating the Nrf2/SLC7A11/GPX4 pathway, thereby suppressing ferroptosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ViTamyloid classifier achieved strong feature-separation metrics, yielding area under the receiver operating characteristic curve (AUROC) and precision-recall curve (AUPRC) values of 0.994/0.958 for CCP, 0.989/0.945 for CGP, 0.992/0.977 for CAA Type 1, and 0.997/0.978 for CAA Type 2. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-brain barrier (BBB) malfunction contributes to pathophysiology of Alzheimer’s disease (AD), yet the mechanisms that confer hippocampal endotheliocytes vulnerability remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nerve Growth Factor (NGF) supports neuronal survival, plasticity, and growth by binding to p75NTR and TrkA receptors. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 6,573 studies in this tag, 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 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 →