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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 35 studies in Risk genes beyond APOE published 2008 (page 1 of 2) · 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.

Elevated cerebrospinal fluid BACE1 activity in incipient Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Archives of neurology 2008-08-01

We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD). 4 key findings →

Design: case-control study Participants: 113 Evidence: moderate

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

The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice

✓ Peer-reviewed alzhub usefulness score 58 out of 100. The Journal of clinical investigation 2008-06-01

Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. 4 key findings →

Evidence: low

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

TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature Genetics 2008-03-30

This study investigated amyotrophic lateral sclerosis, an adult-onset neurological disorder that leads to the degeneration of motor neurons and involves TDP-43 as a key component of ubiquitinated aggregates. 2 key findings →

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

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature medicine 2008-06-01

Alzheimer's disease is the most common dementia and is pathologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques, neuronal injury and low-level, chronic activation of brain immunity. 4 key findings →

Evidence: low

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

Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2008-12-02

Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism is unclear. 4 key findings →

Evidence: low

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

Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Brain research 2008-04-07

We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice. 4 key findings →

Evidence: moderate

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

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

The role of amyloid precursor protein processing by BACE1, the beta-secretase, in Alzheimer disease pathophysiology

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-07-23

Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain. 4 key findings →

Evidence: low

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

Adaptor protein sorting nexin 17 regulates amyloid precursor protein trafficking and processing in the early endosomes

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-02-13

Accumulation of extracellular amyloid beta peptide (Abeta), generated from amyloid precursor protein (APP) processing by beta- and gamma-secretases, is toxic to neurons and is central to the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Alzheimer disease Abeta production in the absence of S-palmitoylation-dependent targeting of BACE1 to lipid rafts

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-12-12

Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase. 4 key findings →

Evidence: low

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

NFkappaB-dependent control of BACE1 promoter transactivation by Abeta42

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-02-08

Beta-amyloid (Abeta) peptides that accumulate in Alzheimer disease are generated from the beta-amyloid precursor protein (betaAPP) by cleavages by beta-secretase BACE1 and by presenilin-dependent gamma-secretase activities. 4 key findings →

Evidence: low

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

Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Archives of neurology 2008-04-01

A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage. 4 key findings →

Evidence: low

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

Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Investigative ophthalmology & visual science 2008-06-19

Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →

Evidence: low

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

MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2008-11-05

MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR). 4 key findings →

Evidence: low

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

The amyloid precursor protein intracellular domain (AICD) as modulator of gene expression, apoptosis, and cytoskeletal dynamics-relevance for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Progress in neurobiology 2008-07-07

Since the discovery of the amyloid precursor protein (APP) in 1987, extensive research has been conducted analyzing the APP-derived beta-amyloid (Abeta) which is found in massive quantities in senile plaques of Alzheimer disease (AD) patients. 4 key findings →

Evidence: low

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

Inhibitors of cathepsin B improve memory and reduce beta-amyloid in transgenic Alzheimer disease mice expressing the wild-type, but not the Swedish mutant, beta-secretase site of the amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2008-01-09

Elucidation of Abeta-lowering agents that inhibit processing of the wild-type (WT) beta-secretase amyloid precursor protein (APP) site, present in most Alzheimer disease (AD) patients, is a logical approach for improving memory deficit in AD. 4 key findings →

Evidence: low

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

Amyloidogenic processing but not amyloid precursor protein (APP) intracellular C-terminal domain production requires a precisely oriented APP dimer assembled by transmembrane GXXXG motifs

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2008-01-16

The beta-amyloid peptide (Abeta) is the major constituent of the amyloid core of senile plaques found in the brain of patients with Alzheimer disease. 4 key findings →

Evidence: low

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

Neprilysin gene expression requires binding of the amyloid precursor protein intracellular domain to its promoter: implications for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. EMBO reports 2008-12-05

Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer disease; however, amyloid metabolism is a dynamic process and enzymic mechanisms exist for Abeta removal. 4 key findings →

Evidence: low

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

Glucocorticoids trigger Alzheimer disease-like pathobiochemistry in rat neuronal cells expressing human tau

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neurochemistry 2008-09-02

Amyloid precursor protein (APP) mis-processing and aberrant tau hyperphosphorylation are causally related to the pathogenesis and neurodegenerative processes that characterize Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Docosahexaenoic acid and the aging brain

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of nutrition 2008-12-01

The dietary essential PUFA docosahexaenoic acid [DHA; 22:6(n-3)] is a critical contributor to cell structure and function in the nervous system, and deficits in DHA abundance are associated with cognitive decline during aging and in neurodegenerative disease. 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. 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