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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 351–375 of 1,618 studies (page 15 of 65) · 28,180 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 1,618 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; 13,658 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.

Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 1992-10-01

Altered processing of the amyloid precursor protein (APP) is a central event in the formation of amyloid deposits in the brains of individuals with Alzheimer's disease. 3 key findings →

Evidence: low

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

Distinct sites of intracellular production for Alzheimer's disease A beta40/42 amyloid peptides

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature medicine 1997-09-01

The Alzheimer amyloid precursor protein (APP) is cleaved by several proteases, the most studied, but still unidentified ones, are those involved in the release of a fragment of APP, the amyloidogenic beta-protein A beta. 4 key findings →

Evidence: low

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

Association of Rare Coding Mutations With Alzheimer Disease and Other Dementias Among Adults of European Ancestry

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA network open 2019-03-01

Some of the unexplained heritability of Alzheimer disease (AD) may be due to rare variants whose effects are not captured in genome-wide association studies because very large samples are needed to observe statistically significant associations. 4 key findings →

Participants: 5,617 Evidence: low

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

Left lateralized cerebral glucose metabolism declines in amyloid-β positive persons with mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 55 out of 100. NeuroImage. Clinical 2018-07-17

Previous publications indicate that Alzheimer's Disease (AD) related cortical atrophy may develop in asymmetric patterns, with accentuation of the left hemisphere. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Cerebral amyloid angiopathy and Alzheimer disease - one peptide, two pathways

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature reviews. Neurology 2019-12-11

The shared role of amyloid-β (Aβ) deposition in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest instance of crosstalk between neurodegenerative and cerebrovascular processes. 4 key findings →

Evidence: low

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

Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer s Research & Therapy 2026-05-07

CSF SDC4 levels were elevated in AD, including the earliest preclinical stages, compared to controls and were closely associated with CSF and imaging biomarkers of amyloid and tau, and CSF biomarkers of neuronal and synaptic injury, astrocytic reactivity and microglial dysregulation. 1 key finding →

Design: cross-sectional Participants: 1,041 Evidence: moderate

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

Plasma Aβ42/Aβ40 determined by mass spectrometry is associated with longitudinal changes in amyloid accumulation, brain atrophy, and conversion to mild cognitive impairment due to Alzheimer’s disease in individuals with subjective cognitive decline: 5-year follow-up of the FACEHBI cohort

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of Prevention of Alzheimer s Disease 2026-01-08

Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →

Design: longitudinal study Participants: 200 Evidence: moderate

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

(11)C-PBR28 binding to translocator protein increases with progression of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurobiology of aging 2016-04-27

This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease. 1 key finding →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Cognitive decline and brain volume loss as signatures of cerebral amyloid-beta peptide deposition identified with Pittsburgh compound B: cognitive decline associated with Abeta deposition

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Archives of neurology 2009-12-01

The in vivo measure of cerebral amyloidosis known as [(11)C]PiB is associated with cross-sectional regionally specific brain atrophy and longitudinal cognitive decline in multiple cognitive domains that occur before the clinical diagnosis of Alzheimer disease. 4 key findings →

Design: cross-sectional Participants: 135 Evidence: moderate

Full summary, score breakdown and related studies → Original source

APOE and BCHE as modulators of cerebral amyloid deposition: a florbetapir PET genome-wide association study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Molecular psychiatry 2013-02-19

Deposition of amyloid-β (Aβ) in the cerebral cortex is thought to be a pivotal event in Alzheimer's disease (AD) pathogenesis with a significant genetic contribution. 3 key findings →

Participants: 555 Evidence: low

Full summary, score breakdown and related studies → Original source

Association of APOE ɛ4 and Plasma p-tau181 with Preclinical Alzheimer’s Disease and Longitudinal Change in Hippocampus Function

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Journal of Alzheimer's Disease 2022-02-01

Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). 3 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-09-01

Apolipoprotein E (apoE), a plasma apolipoprotein that plays a central role in lipoprotein metabolism, is localized in the senile plaques, congophilic angiopathy, and neurofibrillary tangles of Alzheimer disease. 3 key findings →

Evidence: low

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

Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2007-05-01

These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment. 2 key findings →

Evidence: low

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

PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2007-05-01

The SPM analysis showed that patients with MCI had significantly higher [(11)C]PIB uptake vs control subjects in the frontal, parietal, and lateral temporal cortices as well as in the posterior cingulate showing the most prominent differences. 4 key findings →

Participants: 13 Evidence: low

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

From across this tag

10 of the 1,616 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 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 →

Newest studies, as a dated timeline →    Atom feed