ArticleAustin Alzheimer's and Parkinson's disease2014
Cycle on Wheels: Is APP Key to the AppBp1 Pathway?
Article in Austin Alzheimer's and Parkinson's disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Role of Neddylation in Neurodegenerative Diseases.NeuroSci · 2022Review
- Targeting neddylation E2s: a novel therapeutic strategy in cancer.Journal of hematology & oncology · 2021Review
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues.American journal of physiology. Endocrinology and metabolism · 2019Article
- Clinical significance of ubiquilin 1 in gastric cancer.Medicine · 2018Article
- Taming Alzheimer's disease: New perspectives, newer horizons.Iranian journal of neurology · 2017Review
- Overexpression of Ubiquilin-1 Alleviates Alzheimer's Disease-Caused Cognitive and Motor Deficits and Reduces Amyloid-β Accumulation in Mice.Journal of Alzheimer's disease : JAD · 2017Article
- How Research on Human Progeroid and Antigeroid Syndromes Can Contribute to the Longevity Dividend Initiative.Cold Spring Harbor perspectives in medicine · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the gradual loss of the cognitive function due to neuronal death. Currently no therapy is available to slow down, reverse or prevent the disease. Here we analyze the existing data in literature and hypothesize that the physiological function of the Amyloid Precursor Protein (APP) is activating the AppBp1 pathway and this function is gradually lost during the progression of AD pathogenesis. The AppBp1 pathway, also known as the neddylation pathway, activates the small ubiquitin-like protein nedd8, which covalently modifies and switches on Cullin ubiquitin ligases, which are essential in the turnover of cell cycle proteins. Here we discuss how APP may activate the AppBp1 pathway, which downregulates cell cycle markers and protects genome integrity. More investigation of this mechanism-driven hypothesis may provide insights into disease treatment and prevention strategies.
Indexed as
Identifiers
25568892PMC4283775W41666894What 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.