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Research

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

Find studies

Showing 176–200 of 847 studies in Risk genes beyond APOE (page 8 of 34) · 27,380 in the whole library · How the 0–100 score works

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 “Risk genes beyond APOE” covers

Risk genes beyond APOE — Genome-wide studies and individual genes other than APOE that shift Alzheimer's risk.

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.

Generation of Alzheimer beta-amyloid protein in the trans-Golgi network in the apparent absence of vesicle formation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01

beta-amyloid protein (A beta) formation was reconstituted in permeabilized neuroblastoma cells expressing human Alzheimer beta-amyloid precursor protein (beta APP) harboring the Swedish double mutation associated with familial early-onset Alzheimer disease. 4 key findings →

Evidence: low

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

Evidence that the 42- and 40-amino acid forms of amyloid beta protein are generated from the beta-amyloid precursor protein by different protease activities

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

Cerebral deposition of the amyloid beta protein (A beta) is an early and invariant feature of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

The common inhalation anesthetic isoflurane induces apoptosis and increases amyloid beta protein levels

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Anesthesiology 2006-05-01

The common inhalation anesthetic isoflurane has previously been reported to enhance the aggregation and cytotoxicity of the Alzheimer disease-associated amyloid beta protein (Abeta), the principal peptide component of cerebral beta-amyloid deposits. 4 key findings →

Evidence: low

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

Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS medicine 2005-11-15

The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease. 4 key findings →

Evidence: low

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

Neuronal amyloid-β accumulation within cholinergic basal forebrain in ageing and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain : a journal of neurology 2015-03-01

The mechanisms that contribute to selective vulnerability of the magnocellular basal forebrain cholinergic neurons in neurodegenerative diseases, such as Alzheimer's disease, are not fully understood. 4 key findings →

Evidence: low

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

Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-07-01

Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes increase the production of the highly amyloidogenic 42-residue form of amyloid beta-protein (Abeta42) in a variety of cell lines and transgenic mice. 4 key findings →

Evidence: low

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

APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The EMBO journal 2011-04-26

Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and its proteolytic fragments are still poorly understood. 4 key findings →

Evidence: low

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

Mechanisms of Pathogenic Tau and Aβ Protein Spreading in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Frontiers in aging neuroscience 2020-08-27

Alzheimer's disease (AD) is pathologically defined by extracellular accumulation of amyloid-β (Aβ) peptides generated by the cleavage of amyloid precursor protein (APP), strings of hyperphosphorylated Tau proteins accumulating inside neurons known as neurofibrillary tangles (NFTs) and neuronal loss. 4 key findings →

Evidence: low

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

Hydrogen peroxide promotes Abeta production through JNK-dependent activation of gamma-secretase

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2008-04-23

Accumulation of senile plaques composed of amyloid beta-peptide (Abeta) is a pathological hallmark of Alzheimer disease (AD), and Abeta is generated through the sequential cleavage of amyloid precursor protein (APP) by beta- and gamma-secretase. 4 key findings →

Evidence: low

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

Parkinson's disease iron deposition caused by nitric oxide-induced loss of β-amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2015-02-01

Elevation of both neuronal iron and nitric oxide (NO) in the substantia nigra are associated with Parkinson's disease (PD) pathogenesis. 4 key findings →

Evidence: low

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

Cholesterol impairs autophagy-mediated clearance of amyloid beta while promoting its secretion

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Autophagy 2018-06-04

Macroautophagy/autophagy failure with the accumulation of autophagosomes is an early neuropathological feature of Alzheimer disease (AD) that directly affects amyloid beta (Aβ) metabolism. 4 key findings →

Evidence: low

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

The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Autophagy 2021-08-19

Primary dysfunction of autophagy due to Mendelian defects affecting core components of the autophagy machinery or closely related proteins have recently emerged as an important cause of genetic disease. 4 key findings →

Evidence: low

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

Reducing amyloid plaque burden via ex vivo gene delivery of an Abeta-degrading protease: a novel therapeutic approach to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS medicine 2007-08-01

Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Cholesterol alters mitophagy by impairing optineurin recruitment and lysosomal clearance in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular neurodegeneration 2021-03-08

Emerging evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer's disease (AD) pathogenesis. 4 key findings →

Evidence: low

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

Mutational analysis in early-onset familial Alzheimer's disease in Mainland China

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurobiology of aging 2014-02-20

Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 5 key findings →

Participants: 32 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Archives of neurology 2002-09-01

Amyloid plaques, a major pathological feature of Alzheimer disease (AD), are composed of an internal fragment of amyloid precursor protein (APP): the 4-kd amyloid-beta protein (Abeta). 4 key findings →

Evidence: low

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

Glia and their cytokines in progression of neurodegeneration

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurobiology of aging 2005-03-01

A glia-mediated, inflammatory immune response is an important component of the neuropathophysiology of Alzheimer's disease, of the midlife neurodegeneration of Down's syndrome, and of other age-related neurodegenerative conditions. 4 key findings →

Evidence: low

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

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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