Dendrites and axons are delicate neuronal membrane extensions that undergo degeneration after physical injuries. In neurodegenerative diseases, they often degenerate prior to neuronal death. Understanding the mechanisms of neurite degeneration has been an intense focus of neurobiology research in the last two decades. As a result, many discoveries have been made in the molecular pathways that lead to neurite degeneration and the cell-cell interactions responsible for the subsequent clearance of neuronal debris. Drosophila melanogaster has served as a prime in vivo model system for identifying and characterizing the key molecular players in neurite degeneration, thanks to its genetic tractability and easy access to its nervous system. The knowledge learned in the fly provided targets and fuel for studies in other model systems that have further enhanced our understanding of neurodegeneration. In this review, we will introduce the experimental systems developed in Drosophila to investigate injury-induced neurite degeneration, and then discuss the biological pathways that drive degeneration. We will also cover what is known about the mechanisms of how phagocytes recognize and clear degenerating neurites, and how recent findings in this area enhance our understanding of neurodegenerative disease pathology.

树突和轴突是脆弱的神经元膜延伸，在物理损伤后会发生退化。在神经退行性疾病中，它们通常在神经元死亡之前退化。了解神经突变性的机制一直是过去二十年神经生物学研究的重点。因此，在导致神经突变性的分子途径以及负责随后清除神经元碎片的细胞间相互作用方面取得了许多发现。由于其遗传易处理性和易于接近其神经系统，黑腹果蝇已成为识别和表征神经突变性中关键分子参与者的主要体内模型系统。在飞行中学到的知识为其他模型系统的研究提供了目标和燃料，进一步增强了我们对神经退行性疾病的理解。在这篇综述中，我们将介绍在果蝇中开发的实验系统，用于研究损伤引起的神经突变性，然后讨论驱动变性的生物学途径。我们还将介绍吞噬细胞如何识别和清除退化神经突的已知机制，以及该领域的最新发现如何增强我们对神经退行性疾病病理学的理解。