We show that m 6 A modification displays temporal and spatial dynamics during neurodevelopment and aging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Human lumbar CSF patterns of Abeta peptides were analysed by urea-based beta-amyloid sodium dodecyl sulphate polyacrylamide gel electrophoresis with western immunoblot (Abeta-SDS-PAGE/immunoblot). 4 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
51/100
RBC DHA was associated with a positive (improved) global cognition (PACC) rate of change (estimate: 0.011; 95% CI: 0.001, 0.021; P = 0.024). 5 key findings →
Design: longitudinal study Participants: 323 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline. 2 key findings →
Participants: 251 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD. 4 key findings →
Design: longitudinal study Participants: 1,051 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Routine liver–metabolic indices were associated with cognitive performance, while FIB-4 stage showed effect modification by APOE ε4 in relation to both cognition and amyloid PET SUVR. 4 key findings →
Design: longitudinal study Participants: 507 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher AD PRS was associated with increased risks of all-cause dementia (HR: 1.75, 95% CI: 1.70-1.79, P < 0.001) and AD (HR: 2.02, 95% CI: 1.95-2.09, P < 0.001), with stronger effects in women for both outcomes when considering the main AD PRS which was related to APOE4 status. 4 key findings →
Participants: 249 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified several new mutations of MS4A6A with altered AD risks, and discovered specific correlation for some of them with the amount of β-amyloid in cerebrospinal fluid. 5 key findings →
Participants: 734,121 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Since the world population is ageing, dementia is going to be a growing concern. 2 key findings →
Design: meta-analysis Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chain-free SFA and TFA occur in greater amounts in the brains of individuals with AD than in those without AD. 1 key finding →
Design: systematic review Participants: 2,297 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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51/100
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Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →
Design: cross-sectional Participants: 751 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Better cognitive outcome and higher synaptic density in PS2APP mice was predicted by higher TSPO expression at 8 mo. The progression of TSPO activation to 13 mo also showed a moderate association with spared cognition, but amyloidosis did not correlate with the cognitive outcome, regardless of the time point. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Heterogeneity in progression to Alzheimer's disease (AD) poses challenges for both clinical prognosis and clinical trial implementation. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We confirm in a completely independent data set that CR1, CLU, and PICALM are AD susceptibility loci in European ancestry populations. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The results of this study suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate NP formation in combination with the effects of APOE epsilon4. 2 key findings →
Evidence: low
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50/100
The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
50/100
APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results indicate lipid droplet accumulation occurs in human DAM xMGs in AD, but is reduced in TREM2-R47H DAM xMGs, as it occurs secondary to TREM2-mediated changes in plaque proximity and reactivity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 1,611 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Cerebral small vessel disease-induced apolipoprotein E leakage is associated with Alzheimer disease and the accumulation of amyloid beta-protein in perivascular astrocytes
- APOE interacts with ACE2 inhibiting SARS-CoV-2 cellular entry and inflammation in COVID-19 patients
- ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease
- Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path
- Microarray analysis of hippocampal CA1 neurons implicates early endosomal dysfunction during Alzheimer's disease progression
- Electroacupuncture ameliorates beta-amyloid pathology and cognitive impairment in Alzheimer disease via a novel mechanism involving activation of TFEB (transcription factor EB)
- Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease
- Abeta toxicity in Alzheimer's disease: globular oligomers (ADDLs) as new vaccine and drug targets
- Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
- Melatonin reverses the profibrillogenic activity of apolipoprotein E4 on the Alzheimer amyloid Abeta peptide
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 27,780 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.
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 27,780 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 →