27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Precision nutrition is a tailored dietary approach that considers an individual’s genetic and metabolic profile, lifestyle factors, and specific nutritional needs to improve health and potentially modify disease progression. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aims to comprehensively review the role of glial fibrillary acidic protein (GFAP) as a marker of astrocyte activation in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous studies have shown that preeclampsia increases the risk of cerebrovascular and cardiovascular diseases, as well as cognitive impairments, up to evolving dementia in the future. 3 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 globally and is marked by amyloid-β plaque accumulation, decreased brain pH, disrupted metabolism, and increased permeability of the blood-brain barrier. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia and neuroinflammation are implicated in the development and progression of Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglial activation and FR expression in APP/PS1 and P301S transgenic mouse models of AD was measured using flow cytometry. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial activation and subsequent neuroinflammation involves THIK-1 (KCNK13), a Two-Pore Domain (K2P) K+ channel. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This method establishes a platform for high-throughput longitudinal drug screening in immunocompetent human COs that will enable the identification of new therapeutic candidates to modulate Aβ aggregation, glial reactivity, and neurodegeneration. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
At the group level, the resting alpha abnormality in AD comprises two partly nonredundant dimensions: reduced expression and a weaker temporal link between alpha and subsequent multi-rhythm activity. 1 key finding →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are a growing global health burden associated with aging and characterized by progressive neuronal dysfunction, metabolic failure, mitochondrial impairment, oxidative stress, and chronic neuroinflammation. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Together, these findings identify astrocytic TrkB.T as an important regulator of amyloid pathology and synaptic integrity in an AD mouse model. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Maternal microbiome-dependent programming of neuroimmune and metabolic pathways during early development may critically shape sex-specific susceptibility to Alzheimer’s disease (AD) later in life. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological tau accumulation is a hallmark of Alzheimer’s disease (AD), yet its relationship with impaired insulin signaling remains unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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 →