27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The top-down approach to proteomics offers compelling advantages due to the potential to provide complete characterization of protein sequence and post-translational modifications. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nitric oxide (NO) has been implicated in the pathophysiology of a number of neurodegenerative diseases including Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an increasing body evidence pointing to a close integration between the central nervous system (CNS) and immunological functions with lymphocytes playing therein a central role. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The senescence-accelerated mouse (SAM) is an accelerated aging model that was established through phenotypic selection from a common genetic pool of AKR/J strain of mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Wnt/β-catenin signalling plays essential roles in embryonic development as well as tissue homoeostasis in adults. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of neurofibrillary tangles, senile plaques and loss of synapses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, an age-related neurodegenerative disorder, is characterized clinically by a progressive loss of memory and cognitive functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of molecular mimicry was established to explain commonalities of structure which developed in response to evolutionary pressures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation is a major epigenetic modification that regulates gene expression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
By comparing the cerebrospinal fluid (CSF) proteome between Alzheimer's disease (AD) patients and controls, it may be possible to identify proteins that play a role in the disease process and thus to study the pathogenesis of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An increasing body of evidence indicates that oxidative stress and damage play a role in the pathogenesis of a number of diseases associated with neurodegeneration, including Down syndrome (DS), Alzheimer's disease (AD) and Pick's disease (PD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Defects in lysosomal function have been associated with numerous monogenic human diseases typically classified as lysosomal storage diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epigenetic modifications represent mechanisms by which cells may effectively translate multiple signaling inputs into phenotypic outputs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated Tau proteins belong to a family of factors that polymerize tubulin dimers and stabilize microtubules. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE = gene, apoE = protein) plays a central role in plasma lipoprotein metabolism and in lipid transport within tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The brains of Alzheimer's disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of intracellular neurofibrillary tangles (NFT), extracellular senile plaques (SP), and synaptic loss. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies have demonstrated the need for complementing cellular genomic information with specific information on expressed proteins, or proteomics, since the correlation between the two is poor. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an urgent need for Alzheimer's disease (AD) biomarkers-especially in the context of clinical trials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Atherosclerotic phenotypes were significantly accelerated in RGS 5 −/− ApoE −/− mice, as indicated by increased inflammatory mediator expression and apoptosis of endothelial cells and macrophages. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disturbed blood flow (d-flow) occurring in branched and curved arteries promotes endothelial dysfunction and atherosclerosis, in part, by altering gene expression and epigenomic profiles in endothelial cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Atherosclerosis is essentially a vascular inflammatory process in the presence of an excess amount of lipid. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intriguingly, the process is dependent on the presence of B cells and significantly contributes to the development of AAA and the occurrence of aortic rupture. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
LSKL peptide administration was associated with greater aortic elastin fragmentation and lower expression and activity of the TGF-β1-target gene lysyl oxidase like 1 ( LOXL1 ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CTS significantly attenuated atherosclerotic plaque formation and enhanced plaque stability in ApoE −/− mice by inhibiting the expression of lectin‐like ox LDL receptor‐1 ( LOX ‐1) and MMP ‐9, as well as inhibiting reactive oxygen species ( ROS ) generation and NF‐κB activation. 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 27,380 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 →