27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Transactive response DNA-binding protein 43 (TDP-43) aggregation and loss of function are hallmark features of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) among other neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, yet the environmental drivers that accelerate its progression remain poorly defined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution (AirP) exposure is associated with increased Alzheimer’s disease (AD) risk, yet AirP is chemically heterogeneous, complicating identification of shared pathogenic drivers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s Disease (AD) is characterised by the progressive depletion of Acetylcholine (ACh), a neurotransmitter essential for cognition and synaptic communication. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metabotropic glutamate receptors (mGluRs) regulate glutamatergic transmission and have been implicated in diverse neuropsychiatric disorders, but human postmortem evidence remains fragmented. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
DMII provides a metabolomics-based framework for assessing diet-related chronic inflammation using metabolomics data. 4 key findings →
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
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
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
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
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
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
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
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
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
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
Cerebral amyloid angiopathy (CAA), characterized by cerebrovascular amyloid deposition, is strongly associated with Alzheimer’s disease, ischemic injury, and lobar hemorrhages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Variants at the CD2AP locus, which encodes a branched-actin regulator, are associated with late-onset Alzheimer’s disease (AD), and CD2AP-deficient mice show increased blood-brain barrier (BBB) permeability. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of proteins such as amyloid β (Aβ), hyperphosphorylated tau and α-synuclein within the brain alters neural information processing and causes neurodegeneration 1–3 , but how toxic solutes are cleared from the brain remains highly controversial 4,5 . 5 key findings →
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 →