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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 84 studies in Disease mechanisms (page 1 of 4) · 27,380 in the whole library · How the 0–100 score works

Showing 84 studies tagged amyloid-beta — clear

Browse by subject, author or institution

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

Other subjects

Authors

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

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “Disease mechanisms” covers

Disease mechanisms — Cell- and molecule-level research into what actually goes wrong in Alzheimer's and related diseases.

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.

ABI3 and PLCG2 missense variants as risk factors for neurodegenerative diseases in Caucasians and African Americans

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Molecular neurodegeneration 2018-10-11

Using Fisher's exact test, there was significant association of both ABI3_rs616338-T (OR = 1.41, p = 0.044) and PLCG2_rs72824905-G (OR = 0.56, p = 0.008) with AD. 5 key findings →

Design: case-control study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Synaptic markers are associated with cognitive decline after accounting for amyloid burden among an at-risk Alzheimer’s disease cohort

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Scientific Reports 2025-06-03

Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration. 2 key findings →

Design: longitudinal study Evidence: moderate

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

Advanced Glycation End-Products Are Associated With the Presence and Severity of Paratonia in Early Stage Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of the American Medical Directors Association 2017-05-27

From the 144 participants (56.3% female and 43.7% male, with a mean [standard deviation] age of 80.7 [7.7] years), 118 participants were available for final follow-up. 4 key findings →

Design: cohort study Participants: 144 Evidence: moderate

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

Copper subtype of Alzheimer's disease (AD): meta-analyses, genetic studies and predictive value of non-ceruloplasmim copper in mild cognitive impairment conversion to full AD

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) 2014-07-10

Alzheimer's disease (AD) is the most common form of dementia. 2 key findings →

Design: meta-analysis Evidence: high

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

Circulating levels of soluble receptor for advanced glycation end products in Alzheimer disease and vascular dementia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Archives of neurology 2005-11-01

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

Association between advanced glycation end-products and functional performance in Alzheimer's disease and mixed dementia

✓ Peer-reviewed alzhub usefulness score 50 out of 100. International psychogeriatrics 2017-05-25

This study indicates that high AGE levels could be a contributing factor to impaired mobility but lacks evidence for an association with ADL decline in people with early stage AD or mixed dementia. 4 key findings →

Design: cohort study Participants: 144 Evidence: moderate

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

Synaptic proteins predict cognitive decline in Alzheimer's disease and Lewy body dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2016-05-22

Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases. 4 key findings →

Participants: 129 Evidence: low

Full summary, score breakdown and related studies → Original source

Multi-functional role of apolipoprotein E in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in Aging Neuroscience 2025-01-29

Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD). 1 key finding →

Evidence: low

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

APOE2 gene therapy reduces amyloid deposition and improves markers of neuroinflammation and neurodegeneration in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular therapy : the journal of the American Society of Gene Therapy 2024-03-19

Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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