52/100
Maintaining DNA integrity is vital for all cells and organisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Common single nucleotide polymorphisms in the SORL1 gene have been associated with late onset Alzheimer disease (LOAD), but causal variants have not been fully characterized nor has the mechanism been established. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Autophagy is an intracellular degradation pathway that functions in protein and organelle turnover in response to starvation and cellular stress. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The detection of genetic loci associated with Alzheimer's disease (AD) requires large numbers of cases and controls because variant effect sizes are mostly small. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
52/100
Low n-3 polyunsaturated fatty acid (PUFA) status may be associated with neuro-degenerative disorders, in particular Alzheimer's disease, which has been associated with poor dietary fish or n-3 PUFA intake, and low docosahexaenoic acid (DHA) status. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There is a wide interest in biomarkers that capture the burden of detrimental factors as these accumulate with the passage of time, i.e., increasing age. 4 key findings →
Participants: 1,961 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several mutations in the amyloid precursor protein (APP) gene have been found to associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Familial British dementia (FBD), previously designated familial cerebral amyloid angiopathy-British type, is an autosomal dominant disorder of undetermined origin characterized by progressive dementia, spasticity, and cerebellar ataxia, with onset at around the fifth decade of life. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Patients with Alzheimer's disease (AD) have abnormally low positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several studies have reported an association of the apolipoprotein E allele epsilon 4 (APOE*4) to familial and sporadic late-onset Alzheimer's disease (LOAD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The relationship of microglia and astrocytes to deposits of beta-amyloid protein (BAP) was studied in Alzheimer's disease by immunohistochemistry. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Microglial cells closely interact with senile plaques in Alzheimer's disease and acquire the morphological appearance of an activated phenotype. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has become apparent that the intestinal microbiota orchestrates important aspects of our metabolism, immunity, and development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Apolipoprotein E (apoE) alleles determine the age-adjusted relative risk (epsilon4 > epsilon3) for Alzheimer's disease (AD).
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls. 2 key findings →
Design: cross-sectional Participants: 152 Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating research has linked Mediterranean diet (MeDi) adherence with slower cognitive decline and reduced Alzheimer's disease (AD) risk. 4 key findings →
Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source
51/100
Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The early endosome is the first vacuolar compartment along the endocytic pathway. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. 3 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
51/100
APOE genotype is a major genetic risk factor for late-onset Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 1,383 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.
- The cerebral beta-amyloid angiopathies: hereditary and sporadic
- Sex Differences in Neuropathology and Cognitive Behavior in APP/PS1/tau Triple-Transgenic Mouse Model of Alzheimer's Disease
- Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease
- The apolipoprotein epsilon 4 allele in patients with Alzheimer's disease
- Posterior cingulate glucose metabolism, hippocampal glucose metabolism, and hippocampal volume in cognitively normal, late-middle-aged persons at 3 levels of genetic risk for Alzheimer disease
- Early changes in CSF sTREM2 in dominantly inherited Alzheimer's disease occur after amyloid deposition and neuronal injury
- Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease
- Hypoxia due to cardiac arrest induces a time-dependent increase in serum amyloid β levels in humans
- Curcumin restores innate immune Alzheimer's disease risk gene expression to ameliorate Alzheimer pathogenesis
- (11)C-PBR28 binding to translocator protein increases with progression of Alzheimer's disease
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 →