ReviewBiochimica et biophysica acta2007
Dysfunction of amyloid precursor protein signaling in neurons leads to DNA synthesis and apoptosis.
Review in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Region-specific proteomic analysis of aging rhesus macaques following chronic glutamate-carboxypeptidase-II (GCPII) inhibition elucidates potential treatment strategies for sporadic Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- Role of Neddylation in Neurodegenerative Diseases.NeuroSci · 2022Review
- LncRNA RP11-59J16.2 aggravates apoptosis and increases tau phosphorylation by targeting MCM2 in AD.Frontiers in genetics · 2022Article
- Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.Hormones and behavior · 2015Review
- Clearance systems in the brain-implications for Alzheimer disease.Nature reviews. Neurology · 2015Review
- A Unified Hypothesis of Early- and Late-Onset Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2015Review
- Genetic interactions associated with 12-month atrophy in hippocampus and entorhinal cortex in Alzheimer's Disease Neuroimaging Initiative.Neurobiology of aging · 2013Article
- Amyloid-β signals through tau to drive ectopic neuronal cell cycle re-entry in Alzheimer's disease.Journal of cell science · 2013Article
- Efficacy of cyclin dependent kinase 4 inhibitors as potent neuroprotective agents against insults relevant to Alzheimer's disease.PloS one · 2013Article
- Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion.Oxidative medicine and cellular longevity · 2013Review
- Amyloid Precursor Protein Binding Protein-1 Is Up-regulated in Brains of Tg2576 Mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- Cyclin-C-dependent cell-cycle entry is required for activation of non-homologous end joining DNA repair in postmitotic neurons.Cell death and differentiation · 2010Article
- Pathological implications of cell cycle re-entry in Alzheimer disease.Expert reviews in molecular medicine · 2010Review
- Article
- Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons.Neurobiology of aging · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The classic neuropathological diagnostic markers for AD are amyloid plaques and neurofibrillary tangles, but their role in the etiology and progression of the disease remains incompletely defined. Research over the last decade has revealed that cell cycle abnormalities also represent a major neuropathological feature of AD. These abnormalities appear very early in the disease process, prior to the appearance of plaques and tangles; and it has been suggested that neuronal cell cycle regulatory failure may be a significant component of the pathogenesis of AD. The amyloid precursor protein (APP) is most commonly known as the source of the beta-amyloid (Abeta) peptides that accumulate in the brains of patients with AD. However, a large body of work supports the idea that APP is also a signaling receptor. Most recently, it has been shown that familial AD (FAD) mutations in APP or simple overexpression of wild type APP cause dysfunction of APP signaling, resulting in initiation of DNA synthesis in neurons and consequent apoptosis. In this article, we review the evidence that APP has the potential to activate aberrant neuronal cell cycle re-entry in AD, and we describe a signal transduction pathway that may mediate this abnormal activation of the cell cycle.
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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.