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Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 101–125 of 448 studies in Risk genes beyond APOE · free to read (page 5 of 18) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 448 studies, in this order: BibTeX (.bib) · RIS (.ris)

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; 14,058 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.

Life extension factor klotho prevents mortality and enhances cognition in hAPP transgenic mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2015-02-01

Aging is the principal demographic risk factor for Alzheimer disease (AD), the most common neurodegenerative disorder. 4 key findings →

Evidence: low

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

Targeting innate immunity for neurodegenerative disorders of the central nervous system

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurochemistry 2016-09-01

Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. 4 key findings →

Evidence: low

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

Chronic treatment with the gamma-secretase inhibitor LY-411,575 inhibits beta-amyloid peptide production and alters lymphopoiesis and intestinal cell differentiation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2004-01-06

Inhibition of gamma-secretase, one of the enzymes responsible for the cleavage of the amyloid precursor protein (APP) to produce the pathogenic beta-amyloid (Abeta) peptides, is an attractive approach to the treatment of Alzheimer disease. 4 key findings →

Evidence: low

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

Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model 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 1997-02-01

The PDAPP transgenic mouse, which overexpresses human amyloid precursor protein (APP717V-->F), has been shown to develop much of the pathology associated with Alzheimer disease. 4 key findings →

Evidence: low

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

Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of clinical investigation 2004-12-01

Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42). 4 key findings →

Evidence: low

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

Processing of Alzheimer beta/A4 amyloid precursor protein: modulation by agents that regulate protein phosphorylation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1990-08-01

The turnover and processing of the Alzheimer beta/A4 amyloid precursor protein (beta APP) has been studied in PC12 cells after treatment with agents that regulate protein phosphorylation. 4 key findings →

Evidence: low

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

Endoplasmic reticulum and trans-Golgi network generate distinct populations of Alzheimer beta-amyloid peptides

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-01-01

The excessive generation and accumulation of 40- and 42-aa beta-amyloid peptides (Abeta40/Abeta42) in selectively vulnerable brain regions is a major neuropathological feature of Alzheimer's disease. 4 key findings →

Evidence: low

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

Sequential proteolytic processing of the triggering receptor expressed on myeloid cells-2 (TREM2) protein by ectodomain shedding and γ-secretase-dependent intramembranous cleavage

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2013-09-27

Triggering receptor expressed on myeloid cells-2 (TREM2) and its signaling adaptor protein TYROBP/DAP12 play important roles in signal transduction in dendritic cells, osteoclasts, tissue macrophages, and microglia. 4 key findings →

Evidence: low

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

beta Subunits of voltage-gated sodium channels are novel substrates of beta-site amyloid precursor protein-cleaving enzyme (BACE1) and gamma-secretase

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2005-04-11

Sequential processing of amyloid precursor protein (APP) by membrane-bound proteases, BACE1 and gamma-secretase, plays a crucial role in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-12-01

The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism. 4 key findings →

Evidence: low

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

CX3CR1 protein signaling modulates microglial activation and protects against plaque-independent cognitive deficits in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2011-07-19

Aberrant microglial activation has been proposed to contribute to the cognitive decline in Alzheimer disease (AD), but the underlying molecular mechanisms remain enigmatic. 4 key findings →

Evidence: low

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

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

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

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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.

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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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