CSF Aß42 levels were lower, whereas t-tau/Aß42 and p-tau/Aß42 ratios were higher in patients with AD compared with those with FTD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lumbar puncture (LP) is a common way of collecting cerebrospinal fluid (CSF) both in the clinic and in research. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease patients, although amyloid deposition and CSF amyloid changes continued to "cascade", there was no evidence to suggest that amyloid and tau biomarkers predicted each other, although both amyloid deposition and CSF tau progression predicted cognitive decline independently. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-seven iNPH, 27 AD, and 18 controls were included. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Commercial advertising of computerized "brain games" may result in clinicians being asked whether brain games prevent dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The findings indicated that participants felt the training was acceptable, enhanced their awareness, and encouraged them to monitor their thinking abilities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research investigating treatments and interventions for cognitive decline and Alzheimer's disease (AD) suffer due to difficulties in accurately identifying individuals at risk of AD in the pre-symptomatic stages of the disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
All participants had significant increases in independent response frequencies, level of personal satisfaction, and heart rates during program sessions as opposed to baseline or control sessions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
During baseline, the mean frequency of correct target responses was virtually zero. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Investigations of apolipoprotein E (APOE) gene, the major genetic risk modifier for Alzheimer's disease (AD), have yielded significant insights into the pathogenic mechanism. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E (apoE) gene has been implicated in various conditions, most notably Alzheimer's disease and coronary artery disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE gene alleles modify human aging and the response to the diet at many levels with diverse pleotropic effects from gut to brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Apolipoprotein E (ApoE) has become a primary focus of research after the discovery of its strong linkage to Alzheimer's disease (AD), where the ApoE4 variant is the highest genetic risk factor for this disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) has been shown to influence amyloid-β (Aβ) clearance from the brain in an isoform-specific manner. 5 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
39/100
Alzheimer's disease (AD) is a progressive degenerative neurological disorder affecting nearly one in nine elderly people in the United States. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age and apolipoprotein E (ApoE) are the mightiest risk factors for dementia and cardiovascular diseases, but the underlying mechanisms remain unclear. 5 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
Apolipoprotein E (APOE) ε4 gene allele and type 2 diabetes mellitus (T2DM) are prime risk factors for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Population-attributable risk models estimate that up to one-third of Alzheimer's disease (AD) cases may be preventable through risk factor modification. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The allele ε4 of the apolipoprotein E gene (APOE ε4) is the major genetic risk factor for non-dominantly inherited Alzheimer's Disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) is the major cholesterol carrier in the brain, affecting various normal cellular processes including neuronal growth, repair and remodeling of membranes, synaptogenesis, clearance and degradation of amyloid β (Aβ) and neuroinflammation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease, currently affecting over 5 million Americans with projections expected to rise as the population ages. 1 key finding →
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
Genetic and epidemiological studies have found that variations in the amyloid precursor protein (APP) and the apoliopoprotein E (APOE) genes represent major modifiers of the progressive neurodegeneration in Alzheimer's disease (AD). 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →