alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 126–150 of 1,613 studies (page 6 of 65) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 1,613 studies tagged apolipoprotein — clear

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 13,259 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Gene Dose of Apolipoprotein E Type 4 Allele and the Risk of Alzheimer's Disease in Late Onset Families

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Science 1993-08-13

The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature 1991-02-21

To avoid the problems that heterogeneity poses for genetic analysis, the researchers examined the cosegregation of Alzheimer's disease and markers along the long arm of chromosome 21 in a single family. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)

✓ Peer-reviewed alzhub usefulness score 63 out of 100. The Lancet. Neurology 2024-07-26

A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses. 3 key findings →

Design: cross-sectional Participants: 190 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Impact of Reference and Target Region Selection on Amyloid PET SUV Ratios in the Phase 1b PRIME Study of Aducanumab

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2018-05-18

Of the reference regions used, subcortical white matter, cerebellar white matter, and the pons, alone or in combination, generated the largest effect sizes. 5 key findings →

Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Candidate single-nucleotide polymorphisms from a genomewide association study of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Archives of neurology 2007-11-12

Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE. 2 key findings →

Design: case-control study Participants: 753 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly. 2 key findings →

Design: cross-sectional Participants: 54 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Plasma apolipoprotein E and Alzheimer disease risk: the AIBL study of aging

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2011-03-01

Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level. 5 key findings →

Design: cross-sectional Participants: 1,079 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

APOE-[epsilon]2 allele associated with higher prevalence of sporadic Parkinson disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2004-06-01

Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease. 3 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →

Design: longitudinal study Participants: 1,075 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis

✓ Peer-reviewed alzhub usefulness score 62 out of 100. PLoS medicine 2014-09-16

Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. 3 key findings →

Design: case-control study Participants: 10,578 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Clinical predictors of severe cerebral amyloid angiopathy and influence of APOE genotype in persons with pathologically verified Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA neurology 2014-07-01

Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →

Design: longitudinal study Participants: 193 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Plasma levels of beta-amyloid(1-40), beta-amyloid(1-42), and total beta-amyloid remain unaffected in adult patients with hypercholesterolemia after treatment with statins

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Archives of neurology 2004-03-01

This study questions the effect of statins on the processing of amyloid precursor protein in humans. 4 key findings →

Evidence: high

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Altered microbiomes distinguish Alzheimer's disease from amnestic mild cognitive impairment and health in a Chinese cohort

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain, behavior, and immunity 2019-05-04

Recently, several animal studies indicated that the 'gut-brain' axis might contribute to the amyloid deposition of AD. 5 key findings →

Design: cross-sectional Participants: 97 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Altered lysosomal proteins in neural-derived plasma exosomes in preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2015-06-10

Levels of autolysosomal proteins in neurally derived blood exosomes distinguish patients with AD from case controls and appear to reflect the pathology of AD up to 10 years before clinical onset. 4 key findings →

Design: cross-sectional Participants: 26 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Lancet (London, England) 1997-01-01

All indicators of atherosclerosis were associated with dementia (odds ratios ranging from 1.3 to 1.9) and its major subtypes Alzheimer's disease (odds ratios 1.3-1.8) and vascular dementia (odds ratios 1.9-3.2). 4 key findings →

Participants: 284 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Identification of preclinical Alzheimer's disease by a profile of pathogenic proteins in neurally derived blood exosomes: A case-control study

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2014-08-15

Levels of P-S396-tau, P-T181-tau, and Aβ1-42 in extracts of neurally derived blood exosomes predict the development of AD up to 10 years before clinical onset. 2 key findings →

Participants: 57 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Annals of Neurology 1991-10-01

We present here both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of 15 patients with Alzheimer's disease and 9 neuropathologically normal subjects. 4 key findings →

Participants: 15 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

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.

↑ Change the filters

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 →

Newest studies, as a dated timeline →    Atom feed