ReviewMetabolic brain disease2025
Unraveling novel mechanisms of ATP-Binding cassette (ABC) transporter in insulin Resistance-induced amyloidogenesis.
Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic advances.Molecular neurodegeneration · 2026Review
- Understanding the link between lipid and ocular disorders for effective therapy.Archives of medical science : AMS · 2026Article
- Boosting Brain Clean-Up: Can Targeting UPS Genes Offer Neuroprotection?Molecular neurobiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance (IR) impairs glucose uptake and metabolism, whereas amyloidogenesis, the formation of abnormal protein aggregation, forming insoluble fibrils called amyloids, which are linked with numerous neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD), Huntington disease's (HD), Parkinson's disease (PD) and Prion's disease. This review explores how IR promotes amyloidogenesis by disrupting cholesterol homeostasis and enhancing Amyloid beta (Aβ) production and aggregation. Specifically, we examine the role of ATP-binding cassette (ABC) transporters in cholesterol homeostasis along with their impact on insulin signaling pathways, highlights how their dysregulation can lead to IR, a significant contributor to the development of amyloidogenesis, a key factor in causing NDDs. We explore the novel molecular mechanisms linking IR and Aβ aggregation, focusing on the interplay between ABC transporters and Amyloid precursor protein (APP) processing. Furthermore, we also explore emerging evidence linking ABC transporters to oxidative stress, inflammation and mitochondrial dysfunction critical factors in the development of amyloidogenesis. Additionally, this review also discusses potential therapeutic strategies targeting ABC transporters to mitigate IR and reduce amyloid burden by various mechanisms including Insulin receptors/IRS-1 signaling, Phosphatidylinositol3kinase-Protein kinase-B (PI3K/AKT), Mitogen-activated protein kinases (MAPK), c-Jun N-terminal kinase (JNK), Glycogen synthase kinase 3 (GSK3), mammalian Target of Rapamycin (mTOR), Insulin-Degrading Enzyme (IDE), Advanced glycation end products (AGEs), Glucose transporters (GLUTs), Apolipoprotein E (ApoE), Peroxisome proliferator-activated receptors (PPARs), Adiponectin, Mitochondrial dysfunctioning, AMP-activated protein kinase (AMPK) Wingless-related integration site/beta-catenin (Wnt/β-catenin) and Sirtuin1 (SIRT1). These insights provide new possibilities for developing targeted therapies against neurodegenerative diseases associated with IR and amyloid accumulation.
Indexed as
Identifiers
40482009What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.