| First Author | Ghidoni R | Year | 2011 |
| Journal | Neurobiol Aging | Volume | 32 |
| Issue | 8 | Pages | 1435-42 |
| PubMed ID | 19773092 | Mgi Jnum | J:176715 |
| Mgi Id | MGI:5292466 | Doi | 10.1016/j.neurobiolaging.2009.08.013 |
| Citation | Ghidoni R, et al. (2011) Cystatin C is released in association with exosomes: a new tool of neuronal communication which is unbalanced in Alzheimer's disease. Neurobiol Aging 32(8):1435-42 |
| abstractText | It has recently become clear that proteins associated with neurodegenerative disorders can be selectively incorporated into intraluminal vesicles of multivesicular bodies and subsequently released within exosomes. Multiple lines of research support a neuroprotective role for cystatin C in Alzheimer's disease (AD). Herein we demonstrate that cystatin C, a protein targeted to the classical secretory pathway by its signal peptide sequence, is also secreted by mouse primary neurons in association with exosomes. Immunoproteomic analysis using SELDI-TOF MS revealed the presence in exosomes of at least 9 different cystatin C glycoforms. Moreover, the over-expression of familial AD-associated presenilin 2 mutations (PS2 M239I and PS2 T122R) resulted in reduced levels of all cystatin C forms (native and glycosylated) and of amyloid-beta precursor protein (APP) metabolites within exosomes. A better understanding of the mechanisms involved in exosomal processing and release may have important implications for the fight against AD and other neurodegenerative diseases. |
