ArticleJournal of Alzheimer's disease : JAD2008
C-terminal cleavage of the amyloid-beta protein precursor at Asp664: a switch associated with Alzheimer's disease.
Article in Journal of Alzheimer's disease : JAD, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Trial
- Phenserine efficacy in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2010Trial
- The Intricate Role of Caspase-6 and Death Receptor-6 in Neurodegenerative Diseases.Cell biochemistry and biophysics · 2026Review
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Caspase cleavage of APP contributes to amyloid beta-protein induced synaptic injury.bioRxiv : the preprint server for biology · 2025Article
- Amyloidogenesis: What Do We Know So Far?International journal of molecular sciences · 2022Review
- mTOR Attenuation with Rapamycin Reverses Neurovascular Uncoupling and Memory Deficits in Mice Modeling Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Cell Death Related Proteins Beyond Apoptosis in the CNS.Frontiers in cell and developmental biology · 2021Review
- Caspase Activation and Caspase-Mediated Cleavage of APP Is Associated with Amyloid β-Protein-Induced Synapse Loss in Alzheimer's Disease.Cell reports · 2020Article
- The mitochondria-targeted antioxidant MitoQ inhibits memory loss, neuropathology, and extends lifespan in aged 3xTg-AD mice.Molecular and cellular neurosciences · 2019Article
- Protein interacting with Amyloid Precursor Protein tail-1 (PAT1) is involved in early endocytosis.Cellular and molecular life sciences : CMLS · 2019Article
- Palmitoylation of caspase-6 by HIP14 regulates its activation.Cell death and differentiation · 2017Article
- Screening for Small Molecule Inhibitors of Statin-Induced APP C-terminal Toxic Fragment Production.Frontiers in pharmacology · 2017Article
- PAT1 inversely regulates the surface Amyloid Precursor Protein level in mouse primary neurons.BMC neuroscience · 2015Article
- Cytoplasmic SET induces tau hyperphosphorylation through a decrease of methylated phosphatase 2A.BMC neuroscience · 2014Article
- Role of apoptosis in disease.Aging · 2012Review
- Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice.Human molecular genetics · 2012Article
- The small chaperone protein p23 and its cleaved product p19 in cellular stress.Journal of molecular neuroscience : MN · 2012Article
- Association of AICD and Fe65 with Hirano bodies reduces transcriptional activation and initiation of apoptosis.Neurobiology of aging · 2011Article
- Cleavage at the 586 amino acid caspase-6 site in mutant huntingtin influences caspase-6 activation in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
In addition to the proteolytic cleavages that give rise to amyloid-beta (Abeta), the amyloid-beta protein precursor (AbetaPP) is cleaved at Asp664 intracytoplasmically. This cleavage releases a cytotoxic peptide, APP-C31, removes AbetaPP-interaction motifs required for signaling and internalization, and is required for the generation of AD-like deficits in a mouse model of the disease. Although we and others had previously shown that Asp664 cleavage of AbetaPP is increased in AD brains, the distribution of the Asp664-cleaved forms of AbetaPP in non-diseased and AD brains at different ages had not been determined. Confirming previous reports, we found that Asp664-cleaved forms of AbetaPP were increased in neuronal cytoplasm and nuclei in early-stage AD brains but were absent in age-matched, non-diseased control brains and in late-stage AD brains. Remarkably, however, Asp664-cleaved AbetaPP was prominent in neuronal somata and in processes in entorhinal cortex and hippocampus of non-diseased human brains at ages <45 years. Our observations suggest that Asp664 cleavage of AbetaPP may be part of the normal proteolytic processing of AbetaPP in young (<45 years) human brain and that this cleavage is down-regulated with normal aging, but is aberrantly increased and altered in location in early AD.
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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.