| First Author | Wang Z | Year | 2023 |
| Journal | Front Aging Neurosci | Volume | 15 |
| Pages | 1087823 | PubMed ID | 36761179 |
| Mgi Jnum | J:333115 | Mgi Id | MGI:7433340 |
| Doi | 10.3389/fnagi.2023.1087823 | Citation | Wang Z, et al. (2023) Loss of RAB39B does not alter MPTP-induced Parkinson's disease-like phenotypes in mice. Front Aging Neurosci 15:1087823 |
| abstractText | Parkinson's disease (PD) is a common neurodegenerative movement disorder with undetermined etiology. A major pathological hallmark of PD is the progressive degeneration of dopaminergic neurons in the substantia nigra. Loss-of-function mutations in the RAB39B gene, which encodes a neuronal-specific small GTPase RAB39B, have been associated with X-linked intellectual disability and pathologically confirmed early-onset PD in multiple families. However, the role of RAB39B in PD pathogenesis remains elusive. In this study, we treated Rab39b knock-out (KO) mice with MPTP to explore whether RAB39B deficiency could alter MPTP-induced behavioral impairments and dopaminergic neuron degeneration. Surprisingly, we found that MPTP treatment impaired motor activity and led to loss of tyrosine hydroxylase-positive dopaminergic neurons and gliosis in both WT and Rab39b KO mice. However, RAB39B deficiency did not alter MPTP-induced impairments. These results suggest that RAB39B deficiency does not contribute to PD-like phenotypes through compromising dopaminergic neurons in mice; and its role in PD requires further scrutiny. |
