Drumond-Bock Ana Luiza, Blankenship Harris E, Pham Kevin D, Carter Kelsey A, Freeman Willard M, Beckstead Michael J
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104.
Department of Biochemistry and Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
eNeuro. 2025 May 29;12(5). doi: 10.1523/ENEURO.0107-25.2025. Print 2025 May.
The consequences of aging can vary dramatically between different brain regions and cell types. In the ventral midbrain, dopaminergic neurons develop physiological deficits with normal aging that likely convey susceptibility to neurodegeneration. While nearby GABAergic neurons are thought to be more resilient, decreased GABA signaling in other areas nonetheless correlates with age-related cognitive decline and the development of degenerative diseases. Here, we used two novel cell type-specific translating ribosome affinity purification models to elucidate the impact of healthy brain aging on the molecular profiles of dopamine and GABA neurons in the ventral midbrain. By analyzing differential gene expression from young adult (7-10 months) and old (21-24 months) mice, we detected commonalities in the aging process in both neuronal types, including increased inflammatory responses and upregulation of pro-survival pathways. Both cell types also showed downregulation of genes involved in synaptic connectivity and plasticity. Intriguingly, genes involved in serotonergic synthesis were upregulated with age in GABA neurons and not dopamine-releasing cells. In contrast, dopaminergic neurons showed alterations in genes connected with mitochondrial function and calcium signaling, which were markedly downregulated in male mice. Sex differences were detected in both neuron types, but in general were more prominent in dopamine neurons. Multiple sex effects correlated with the differential prevalence for neurodegenerative diseases such as Parkinson's and Alzheimer's seen in humans. In summary, these results provide insight into the connection between non-pathological aging and susceptibility to neurodegenerative diseases involving the ventral midbrain, and identify molecular phenotypes that could underlie homeostatic maintenance during normal aging.
衰老的后果在不同脑区和细胞类型之间可能有显著差异。在腹侧中脑,多巴胺能神经元随着正常衰老会出现生理缺陷,这可能使它们易患神经退行性变。虽然附近的γ-氨基丁酸能神经元被认为更具弹性,但其他区域γ-氨基丁酸信号的减少与年龄相关的认知衰退和退行性疾病的发展相关。在这里,我们使用了两种新型的细胞类型特异性翻译核糖体亲和纯化模型,以阐明健康脑衰老对腹侧中脑多巴胺能和γ-氨基丁酸能神经元分子谱的影响。通过分析年轻成年(7 - 10个月)和老年(21 - 24个月)小鼠的差异基因表达,我们在两种神经元类型的衰老过程中检测到了共性,包括炎症反应增加和促生存途径的上调。两种细胞类型还显示出参与突触连接和可塑性的基因下调。有趣的是,参与血清素合成的基因在γ-氨基丁酸能神经元中随年龄上调,而在多巴胺释放细胞中则不然。相比之下,多巴胺能神经元显示出与线粒体功能和钙信号相关的基因发生改变,这些基因在雄性小鼠中明显下调。在两种神经元类型中都检测到了性别差异,但总体上在多巴胺能神经元中更明显。多种性别效应与人类中帕金森病和阿尔茨海默病等神经退行性疾病的不同患病率相关。总之,这些结果为非病理性衰老与涉及腹侧中脑的神经退行性疾病易感性之间的联系提供了见解,并确定了可能是正常衰老过程中稳态维持基础的分子表型。