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Research

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

Find studies

Showing 626–650 of 847 studies in Risk genes beyond APOE (page 26 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.

Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of cell biology 2002-03-18

We studied the effect of microtubule-associated tau protein on trafficking of vesicles and organelles in primary cortical neurons, retinal ganglion cells, and neuroblastoma cells. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neuro-inflammation induced by lipopolysaccharide causes cognitive impairment through enhancement of beta-amyloid generation

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of neuroinflammation 2008-08-29

This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Frontiers in genetics 2014-04-23

The goal of this review is to discuss how behavioral tests in mice relate to the pathological and neuropsychological features seen in human Alzheimer's disease (AD), and present a comprehensive analysis of the temporal progression of behavioral impairments in commonly used AD mouse models that contain mutations in amyloid precursor protein (APP). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

PINK1- and Parkin-mediated mitophagy at a glance

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Cell Science 2012-02-15

Recently, work in cultured cells has shown that Parkin can mediate autophagy of damaged mitochondria (termed mitophagy) (Narendra et al., 2008) downstream of PINK1 (Geisler et al., 2010a; Matsuda et al., 2010; Narendra et al., 2010b; Vives-Bauza et al., 2010). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

α-Synuclein Membrane Interactions and Lipid Specificity

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Biological Chemistry 2000-11-01

With the discovery of missense mutations (A53T and A30P) in alpha-synuclein (alpha-Syn) in several families with early onset familial Parkinson's disease, alpha-Syn aggregation and fibril formation have been thought to play a role in the pathogenesis of alpha-synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain pathology (Zurich, Switzerland) 2003-10-01

Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. 4 key findings →

Evidence: low

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

Basal forebrain cholinergic dysfunction in Alzheimer's disease--interrelationship with beta-amyloid, inflammation and neurotrophin signaling

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurochemical research 2005-06-01

Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks. 4 key findings →

Evidence: low

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

Molecular basis of neuroprotective activities of rasagiline and the anti-Alzheimer drug TV3326 [(N-propargyl-(3R)aminoindan-5-YL)-ethyl methyl carbamate]

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cellular and molecular neurobiology 2001-12-01

Rasagiline (N-propargyl-1-(R)-aminoindan) is a selective, irreversible monoamine oxidase B (MAO B) inhibitor which has been developed as an anti-Parkinson drug. 4 key findings →

Evidence: low

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

Downregulated miR-29c correlates with increased BACE1 expression in sporadic Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International journal of clinical and experimental pathology 2015-02-01

Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD) which is characterized by the accumulation of plaques formed of short β-amyloid (APPβ) peptides. 4 key findings →

Evidence: low

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

Treatment strategies targeting amyloid β-protein

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cold Spring Harbor perspectives in medicine 2012-09-01

With the advent of the key discovery in the mid-1980s that the amyloid β-protein (Aβ) is the core constituent of the amyloid plaque pathology found in Alzheimer disease (AD), an intensive effort has been underway to attempt to mitigate its role in the hope of treating the disease. 3 key findings →

Evidence: low

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

High levels of Alzheimer beta-amyloid precursor protein (APP) in children with severely autistic behavior and aggression

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of child neurology 2006-06-01

Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication. 4 key findings →

Evidence: low

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

Engineered butyrate-producing yeasts mitigate Alzheimer-associated phenotypes

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Signal Transduction and Targeted Therapy 2025-11-16

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →

Evidence: low

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

Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production

✓ Peer-reviewed alzhub usefulness score 39 out of 100. eLife 2025-02-11

Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →

Evidence: low

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

TBG096 Ameliorates Memory Deficiency in AD Mouse Model via Promoting Neurogenesis and Regulation of Hsc70/HK2/PKM2/LAMP2A Signaling Pathway

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International Journal of Molecular Sciences 2025-03-20

In previous studies, we isolated a series of novel gentisides with nerve growth factor (NGF)-mimic activities from Gentiana rigescens Franch and conducted continuous structure–activity relationship (SAR) studies. 5 key findings →

Evidence: low

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

↑ 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 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