41/100
PLCG2 expression is restricted primarily to microglia and granule cells of the dentate gyrus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
41/100
Hundreds of proteins are known to be citrullinated and hypercitrullination is associated with autoimmune diseases including rheumatoid arthritis (RA), lupus, ulcerative colitis (UC), Alzheimer's disease, multiple sclerosis (MS), and certain cancers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In BriefIn the search for biomarkers of synapse loss associated with Alzheimer's disease (AD), we used shotgun proteomics to identify a panel of 9 synaptic proteins detectable in human cerebrospinal fluid (CSF).Expression at the human synapse was verified using super resolution microscopy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We devise a conceptually different computational framework based on a holistic view, where single-cell datasets are used to infer global, large-scale regulatory networks. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE), a key lipid transport protein in the brain, is predominantly produced by astrocytes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) genotype determines Alzheimer's disease (AD) susceptibility, with the APOE ε4 allele being an established risk factor for late-onset AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ample evidence suggests that ApoE4 induces microglial dysregulation and impedes Aβ clearance in AD, but the direct neuronal effects of ApoE variants are poorly studied. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Episodic memory impairment is the hallmark symptom of Alzheimer's Disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common type of dementia and, after age, the greatest risk factor for developing AD is the allelic variation of apolipoprotein E (ApoE), with homozygote carriers of the ApoE4 allele having an up to 12-fold greater risk of developing AD than noncarriers. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is well established that sporadic Alzheimer's disease (AD) is polygenic with common and rare genetic variation alongside environmental factors contributing to disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, neuropsychiatric disorders, and related traits have highly complex etiologies but are also highly heritable and identifying the causal genes and biological pathways underlying these traits may advance the development of treatments and preventive strategies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Atrial fibrillation (AF) is the most common heart rhythm disorder worldwide and may have serious cardiovascular health consequences. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The accumulation of aggregated amyloid β (Aβ) peptides in the brain is deeply involved in Alzheimer disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It becomes increasingly important in using genome-wide association studies (GWAS) to select important genetic information associated with qualitative or quantitative traits. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Human longevity is a complex phenotype resulting from the combinations of context-dependent gene-environment interactions that require analysis as a dynamic process in a cohesive ecological and evolutionary framework. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is the fourth major cause of death in the elderly following cancer, heart disease and cerebrovascular disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The biological markers of aging used to predict physical health status in older people are of great interest. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is considered a polygenic disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prediction of disease risk is an essential part of preventative medicine, often guiding clinical management. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has a very strong genetic component, whose characterization has become an essential part of efforts to understand the pathophysiological processes of the disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function and iron accumulation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia, the brain-resident immune cells, are critically involved in many physiological and pathological brain processes, including neurodegeneration. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2) genes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →