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Vol. 10, No. 1-4, 2012
Issue release date: April 2012
Section title: Paper
Free Access
Neurodegenerative Dis 2012;10:60–63
(DOI:10.1159/000332815)

A Persistent Stress Response to Impeded Axonal Transport Leads to Accumulation of Amyloid-β in the Endoplasmic Reticulum, and Is a Probable Cause of Sporadic Alzheimer’s Disease

Muresan V. · Muresan Z.
Department of Pharmacology and Physiology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, N.J., USA
email Corresponding Author

Zoia Muresan

Department of Pharmacology and Physiology

University of Medicine and Dentistry of New Jersey, New Jersey Medical School

185 South Orange Avenue, MSB, I-665, Newark, NJ 07101-1709 (USA)

Tel. +1 973 972 4385, E-Mail muresazo@umdnj.edu


References

  1. Herrup K: Reimagining Alzheimer’s disease – An age-based hypothesis. J Neurosci 2010;30:16755–16762.
  2. Muresan V, Muresan Z: Is abnormal axonal transport a cause, a contributing factor or a consequence of the neuronal pathology in Alzheimer’s disease? Future Neurol 2009;4:761–773.
  3. Qi Y, Wang JK, McMillian M, Chikaraishi DM: Characterization of a CNS cell line, CAD, in which morphological differentiation is initiated by serum deprivation. J Neurosci 1997;17:1217–1225.
  4. Muresan V, Varvel NH, Lamb BT, Muresan Z: The cleavage products of amyloid-beta precursor protein are sorted to distinct carrier vesicles that are independently transported within neurites. J Neurosci 2009;29:3565–3578.
  5. Muresan Z, Muresan V: A phosphorylated, carboxy-terminal fragment of beta-amyloid precursor protein localizes to the splicing factor compartment. Hum Mol Genet 2004;13:475–488.
  6. Muresan Z, Muresan V: c-Jun NH2-terminal kinase-interacting protein-3 facilitates phosphorylation and controls localization of amyloid-beta precursor protein. J Neurosci 2005;25:3741–3751.
  7. Muresan Z, Muresan V: Coordinated transport of phosphorylated amyloid-beta precursor protein and c-Jun NH2-terminal kinase-interacting protein-1. J Cell Biol 2005;171:615–625.
  8. Muresan Z, Muresan V: Neuritic deposits of amyloid-β peptide in a subpopulation of central nervous system-derived neuronal cells. Mol Cell Biol 2006;26:4982–4997.
  9. Muresan Z, Muresan V: The amyloid-beta precursor protein is phosphorylated via distinct pathways during differentiation, mitosis, stress, and degeneration. Mol Biol Cell 2007;18:3835–3844.
  10. Muresan Z, Muresan V: Seeding neuritic plaques from the distance: a possible role for brainstem neurons in the development of Alzheimer’s disease pathology. Neurodegener Dis 2008;5:250–253.

    External Resources

  11. Gouras GK, Tsai J, Naslund J, Vincent B, Edgar M, Checler F, Greenfield JP, Haroutunian V, Buxbaum JD, Xu H, Greengard P, Relkin NR: Intraneuronal abeta42 accumulation in human brain. Am J Pathol 2000;156:15–20.
  12. Muresan Z, Muresan V: The phosphorylated, carboxy-terminal fragments of amyloid-β precursor protein are targeted to multiple intraneuronal locations by destination-specific molecular motors and adaptor proteins. Annu Meet Soc Neurosci, Chicago, October 17–21, 2009.
  13. Muresan Z, Muresan V: Kinesin-1 is a signaling protein that recruits active kinase complexes and directly participates in substrate phosphorylation. Annu Meet Am Soc Cell Biol, San Francisco, December 13–17, 2008.
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  19. He W, Lu Y, Qahwash I, Hu XY, Chang A, Yan R: Reticulon family members modulate bace1 activity and amyloid-beta peptide generation. Nat Med 2004;10:959–965.
  20. Tu H, Nelson O, Bezprozvanny A, Wang Z, Lee SF, Hao YH, Serneels L, De Strooper B, Yu G, Bezprozvanny I: Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer’s disease-linked mutations. Cell 2006;126:981–993.