| First Author | Lim EF | Year | 2017 |
| Journal | Neurobiol Aging | Volume | 53 |
| Pages | 138-149 | PubMed ID | 28185662 |
| Mgi Jnum | J:243140 | Mgi Id | MGI:5907770 |
| Doi | 10.1016/j.neurobiolaging.2017.01.006 | Citation | Lim EF, et al. (2017) AlphaB-crystallin expression correlates with aging deficits in the peripheral nervous system. Neurobiol Aging 53:138-149 |
| abstractText | In an effort to identify factors that contribute to age-related deficits in the undamaged and injured peripheral nervous system (PNS), we noted that Brady and colleagues found that mice null for a small heat shock protein called alphaB-crystallin (alphaBC) developed abnormalities early in life that are reminiscent of aging pathologies. Because of our observation that alphaBC protein levels markedly reduce as wild-type mice age, we investigated whether the crystallin plays a role in modulating age-related deficits in the uninjured and damaged PNS. We show here that the presence of alphaBC correlates with maintenance of myelin sheath thickness, reducing macrophage presence, sustaining lipid metabolism, and promoting remyelination following peripheral nerve injury in an age-dependent manner. More specifically, animals null for alphaBC displayed a higher frequency of thinly myelinated axons, enhanced presence of Iba1+ macrophages, and fewer immunoreactive profiles of the cholesterol biosynthesis enzyme, squalene monooxygenase, before and after sciatic nerve crush injury. These findings thus suggest that alphaBC plays a protective and beneficial role in the aging PNS. |
