ArticlePloS one2013
An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach.International journal of molecular sciences · 2023Review
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- Intracellular accumulation of tau oligomers in astrocytes and their synaptotoxic action rely on Amyloid Precursor Protein Intracellular Domain-dependent expression of Glypican-4.Progress in neurobiology · 2023Article
- The US9-Derived Protein gPTB9TM Modulates APP Processing Without Targeting Secretase Activities.Molecular neurobiology · 2023Article
- Phosphorylation Signaling in APP Processing in Alzheimer's Disease.International journal of molecular sciences · 2019Review
- Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.Journal of Alzheimer's disease : JAD · 2018Review
- LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent.eLife · 2017Article
- The Intersection of NGF/TrkA Signaling and Amyloid Precursor Protein Processing in Alzheimer's Disease Neuropathology.International journal of molecular sciences · 2017Review
- Amyloid Precursor Protein (APP) May Act as a Substrate and a Recognition Unit for CRL4CRBN and Stub1 E3 Ligases Facilitating Ubiquitination of Proteins Involved in Presynaptic Functions and Neurodegeneration.The Journal of biological chemistry · 2016Article
- NGF controls APP cleavage by downregulating APP phosphorylation at Thr668: relevance for Alzheimer's disease.Aging cell · 2016Article
- Amyloid-β precursor protein: Multiple fragments, numerous transport routes and mechanisms.Experimental cell research · 2015Review
- The ITM2B (BRI2) gene is a target of BCL6 repression: Implications for lymphomas and neurodegenerative diseases.Biochimica et biophysica acta · 2015Article
- APP intracellular domain acts as a transcriptional regulator of miR-663 suppressing neuronal differentiation.Cell death & disease · 2015Article
- Article
- Danish and British dementia ITM2b/BRI2 mutations reduce BRI2 protein stability and impair glutamatergic synaptic transmission.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mutations in Amyloid-ß Precursor Protein (APP) and BRI2/ITM2b genes cause Familial Alzheimer and Danish Dementias (FAD/FDD), respectively. APP processing by BACE1, which is inhibited by BRI2, yields sAPPß and ß-CTF. ß-CTF is cleaved by gamma-secretase to produce Aß. A knock-in mouse model of FDD, called FDDKI, shows deficits in memory and synaptic plasticity, which can be attributed to sAPPß/ß-CTF but not Aß. We have investigated further the pathogenic function of ß-CTF focusing on Thr(668) of ß-CTF because phosphorylation of Thr(668) is increased in AD cases. We created a knock-in mouse bearing a Thr(668)Ala mutation (APP(TA) mice) that prevents phosphorylation at this site. This mutation prevents the development of memory and synaptic plasticity deficits in FDDKI mice. These data are consistent with a role for the carboxyl-terminal APP domain in the pathogenesis of dementia and suggest that averting the noxious role of Thr(668) is a viable therapeutic strategy for human dementias.
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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.